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Hypertension: HELP
Articles by Adam T. Whaley-Connell
Based on 38 articles published since 2008
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Between 2008 and 2019, Adam Whaley-Connell wrote the following 38 articles about Hypertension.
 
+ Citations + Abstracts
Pages: 1 · 2
1 Editorial Novel therapeutics in hypertension and kidney disease. 2015

Sperati, C John / Whaley-Connell, Adam. ·aDepartment of Medicine, Division of Nephrology, Johns Hopkins University School of Medicine, Baltimore, Maryland bResearch Service, Harry S Truman Memorial Veterans Hospital and the University of Missouri-Columbia School of Medicine cDepartment of Internal Medicine, Divisions of Nephrology and Hypertension and Endocrinology and Metabolism, Columbia, Missouri, USA. ·Curr Opin Nephrol Hypertens · Pubmed #26181780.

ABSTRACT: -- No abstract --

2 Editorial Novel interventions for resistant hypertension. 2013

Whaley-Connell, Adam. · ·Curr Opin Nephrol Hypertens · Pubmed #23921565.

ABSTRACT: -- No abstract --

3 Editorial Metabolic impact of adding a thiazide diuretic to captopril. 2013

Whaley-Connell, Adam / Sowers, James R. · ·Hypertension · Pubmed #23424231.

ABSTRACT: -- No abstract --

4 Editorial Initial choice of antihypertensive on long-term cardiovascular outcomes in CKD. 2012

Whaley-Connell, Adam / Sowers, James R. · ·Clin J Am Soc Nephrol · Pubmed #22595830.

ABSTRACT: -- No abstract --

5 Editorial The kaliuretic impact of cicletanine compared to hydrochlorothiazide. 2012

Whaley-Connell, Adam / Sowers, James R. · ·J Hypertens · Pubmed #22418907.

ABSTRACT: -- No abstract --

6 Editorial Indices of obesity and cardiometabolic risk. 2011

Whaley-Connell, Adam / Sowers, James R. · ·Hypertension · Pubmed #22025378.

ABSTRACT: -- No abstract --

7 Editorial Is it time to target prehypertension. 2010

Whaley-Connell, Adam / Sowers, James R. · ·Cardiovasc Ther · Pubmed #21050419.

ABSTRACT: -- No abstract --

8 Editorial Hypertension and insulin resistance. 2009

Whaley-Connell, Adam / Sowers, James R. · ·Hypertension · Pubmed #19635987.

ABSTRACT: -- No abstract --

9 Editorial Aldosterone and hypertension in the cardiometabolic syndrome. 2008

Stas, Sameer / Whaley-Connell, Adam T / Sowers, James R. · ·J Clin Hypertens (Greenwich) · Pubmed #18256573.

ABSTRACT: -- No abstract --

10 Editorial Obesity, insulin resistance, and nocturnal systolic blood pressure. 2008

Whaley-Connell, Adam / Sowers, James R. · ·Hypertension · Pubmed #18212271.

ABSTRACT: -- No abstract --

11 Review Obesity and insulin resistance in resistant hypertension: implications for the kidney. 2015

Rao, Akhilesh / Pandya, Vishwam / Whaley-Connell, Adam. ·Division of Nephrology and Hypertension, Department of Internal Medicine, University of Missouri-Columbia School of Medicine, Columbia, MO; and Harry S. Truman Memorial Veterans Hospital. ·Adv Chronic Kidney Dis · Pubmed #25908470.

ABSTRACT: There is recognition that the obesity epidemic contributes substantially to the increasing incidence of CKD and resistant hypertension (HTN). The mechanisms by which obesity promotes resistance are an area of active interest and intense investigation. It is thought that increases in visceral adiposity lead to a proinflammatory, pro-oxidative milieu that promote resistance to the metabolic actions of insulin. This resistance to insulin at the level of skeletal muscle tissue impairs glucose disposal/utilization through actions on the endothelium that include vascular rarefaction, reductions in vascular relaxation, and vascular remodeling. Insulin resistance derived from increased adipose tissue and obesity has system-wide implications for other tissue beds such as the kidney that affects blood pressure regulation. The additional autocrine and paracrine activities of adipose tissue contribute to inappropriate activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system that promote kidney microvascular remodeling, stiffness, and sodium (Na(+)) retention that in turn promote HTN and in the CKD patient, resistance. In this review, we will summarize the important mechanisms that link obesity to CKD as they relate to resistant HTN.

12 Review Mineralocorticoid and apparent mineralocorticoid syndromes of secondary hypertension. 2015

Ardhanari, Sivakumar / Kannuswamy, Rohini / Chaudhary, Kunal / Lockette, Warren / Whaley-Connell, Adam. ·Department of Medicine, University of Missouri-Columbia School of Medicine, Columbia, MO; Division of Cardiovascular Medicine, University of Missouri-Columbia School of Medicine, Columbia, MO; Department of Pathology and Anatomical Sciences, University of Missouri, Columbia, MO; Division of Nephrology and Hypertension, University of Missouri-Columbia School of Medicine, Columbia, MO; Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO; and Division of Endocrinology and Metabolism, University of Missouri-Columbia School of Medicine, Columbia, MO. ·Adv Chronic Kidney Dis · Pubmed #25908467.

ABSTRACT: The mineralocorticoid aldosterone is a key hormone in the regulation of plasma volume and blood pressure in man. Excessive levels of this mineralocorticoid have been shown to mediate metabolic disorders and end-organ damage more than what can be attributed to its effects on blood pressure alone. Inappropriate excess levels of aldosterone contribute significantly to the cardiorenal metabolic syndrome and target organ injury that include atherosclerosis, myocardial hypertrophy, fibrosis, heart failure, and kidney disease. The importance of understanding the role of excess mineralocorticoid hormones such as aldosterone in resistant hypertension and in those with secondary hypertension should be visited. Primary aldosteronism is one of the commonly identified causes of hypertension and is treatable and/or potentially curable. We intend to review the management of mineralocorticoid-induced hypertension in the adult population along with other disease entities that mimic primary aldosteronism.

13 Review Diabetic kidney disease and the cardiorenal syndrome: old disease, new perspectives. 2013

Jindal, Ankur / Garcia-Touza, Mariana / Jindal, Nidhi / Whaley-Connell, Adam / Sowers, James R. ·Hospital Medicine, Department of Internal Medicine, University of Missouri, One Hospital Drive, Columbia, MO 65212, USA; Diabetes and Cardiovascular Research Center, University of Missouri, One Hospital Drive, Columbia, MO 65212, USA. ·Endocrinol Metab Clin North Am · Pubmed #24286950.

ABSTRACT: In this article, the literature is reviewed regarding the role of blood pressure variability and nocturnal nondipping of blood pressure as well as the presence of diabetic kidney disease (DKD), in the absence of albuminuria, as risk predictors for progressive DKD. The importance of glycemic and blood pressure control in patients with diabetes and chronic kidney disease, and the use of oral hypoglycemic agents and antihypertensive agents in this patient cohort, are also discussed.

14 Review Novel role for the incretins in blood pressure regulation. 2012

Yerram, Preethi / Whaley-Connell, Adam. ·Division of Nephrology and Hypertension, Department of Internal Medicine, University of Missouri-Columbia School of Medicine, Columbia, Missouri 65212, USA. yerramp@health.misouri.edu ·Curr Opin Nephrol Hypertens · Pubmed #22871675.

ABSTRACT: PURPOSE OF REVIEW: Incretin-based therapies are currently being used in the treatment of type 2 diabetes mellitus (T2DM). Apart from glycemic control, these agents have been shown to have multiple extra-pancreatic effects, including their role in blood pressure (BP) regulation. This article will review the origins of incretins, the incretin axis, possible mechanisms of antihypertensive effect of these agents, as well as the recent evidence. RECENT FINDINGS: Preclinical and clinical studies demonstrate the antihypertensive effects of glucagon-like peptide-1 (GLP-1) and its analogs in patients with T2DM and hypertension. This effect seems to be mediated through vasodilatation as well as modulation of renal sodium handling causing natriuresis, although the exact mechanisms are not fully known. SUMMARY: Incretin-based therapies are emerging as a novel class of hypoglycemic agents that display antihypertensive properties. Given the small decreases in BP, it is unlikely that these agents will be used as stand-alone antihypertensive agents, but they may be an attractive option in patients with T2DM and hypertension.

15 Review Oxidative stress in the cardiorenal metabolic syndrome. 2012

Whaley-Connell, Adam / Sowers, James R. ·Diabetes and Cardiovascular Center, Harry S Truman VA Medical Center and the University of Missouri-Columbia School of Medicine, Columbia, MO 65213, USA. whaleyconnella@health.missouri.edu ·Curr Hypertens Rep · Pubmed #22581415.

ABSTRACT: Excess visceral adiposity contributes to inappropriate activation of the renin-angiotensin-aldosterone system despite a state of volume expansion and of salt retention that contributes to subclinical elevations of pro-oxidant mechanisms. These adverse effects are mediated by excess generation of reactive oxygen species (ROS) and diminished antioxidant defense mechanisms. Excess tissue (i.e., skeletal muscle, liver, heart) free oxygen radicals contribute to impairments in the insulin-dependent metabolic signaling pathways that regulate glucose utilization/disposal and systemic insulin sensitivity. The generation of ROS is required for normal cell signaling and physiological responses. It is a loss of redox homeostasis that results in a proinflammatory/profibrotic milieu that promotes impairments in insulin metabolic signaling, reduced endothelial-mediated vasorelaxation, and associated cardiovascular and renal structural and functional abnormalities. These maladaptive processes are increasingly recognized as important in the progression of hypertension in the cardiorenal metabolic phenotype. There is increasing evidence to support a critical role for Ang II signaling through the AT(1)R and aldosterone actions through the MR in conjunction with an altered redox-mediating impaired endothelial, cardiac and renal function in this metabolic phenotype. There are emerging clinical data that indicate that therapies that target the renin angiotensin-aldosterone system (RAAS) also attenuate oxidative stress, and improve endothelial, cardiac and renal functions, which collectively contribute to reductions in hypertension.

16 Review Atherosclerotic renovascular hypertension: current trends in diagnosis and management. 2011

Chaudhary, Kunal / Botdorf, Joshua / Whaley-Connell, Adam. ·Department of Internal Medicine, Division of Nephrology, University of Missouri School of Medicine, USA. chaudharyk@health.missouri.edu ·Mo Med · Pubmed #21462609.

ABSTRACT: Reno vascular hypertension (RVH) is an important challenge for clinicians managing patients with hypertension. With recent advances in imaging techniques, the diagnosis and recognition of Renal artery stenosis (RAS) has increased resulting in a 3-4 fold increase in endovascular procedures. Recent prospective, randomized trials have demonstrated equivocal results for interventions and a third trial is under way. In managing such patients, clinicians need to consider the risk-benefit of expensive and invasive workup and interventions.

17 Review Resistant hypertension in the high-risk metabolic patient. 2011

Chaudhary, Kunal / Buddineni, J P / Nistala, Ravi / Whaley-Connell, Adam. ·Harry S. Truman Hospital, University of Missouri Health Sciences Center, 800 Hospital Drive, Columbia, MO 65201, USA. chaudharyk@health.missouri.edu ·Curr Diab Rep · Pubmed #20941645.

ABSTRACT: The metabolic syndrome is a constellation of metabolic and vascular abnormalities that include insulin resistance with compensatory hyperinsulinemia, central or visceral obesity, hypertension, dyslipidemia, microalbuminuria, and oxidative stress as well as prothrombotic and inflammatory abnormalities that contribute to a hypercoagulable state and systemic endothelial dysfunction. Visceral adipose tissue is now known to secrete into the circulation a number of protein and nonprotein factors that regulate glucose metabolism in traditional insulin-sensitive tissue as well as nontraditional insulin-sensitive tissue including cardiovascular tissue. Collectively, this constellation of factors that lead to metabolic dysregulation contributes to a substantial risk for adverse cardiovascular and renal outcomes. The development of a particularly resistant form of hypertension in these individuals can be attributed to a number of factors including vasoconstriction from increased sympathetic activation, proinflammatory cytokines, and inappropriate activation of the renin-angiotensin-aldosterone system. The management of hypertension in such patients can be challenging and generally requires nonpharmacologic as well as pharmacologic interventions.

18 Review The emerging role of biomarkers in diabetic and hypertensive chronic kidney disease. 2010

Chaudhary, Kunal / Phadke, Gautam / Nistala, Ravi / Weidmeyer, Charles E / McFarlane, Samy I / Whaley-Connell, Adam. ·Department of Internal Medicine, Division of Nephrology and Hypertension, University of Missouri-Columbia School of Medicine, CE417, DC043.0, Five Hospital Drive, Columbia, MO 65212, USA. ·Curr Diab Rep · Pubmed #20425065.

ABSTRACT: Currently used measures to assess kidney function and injury are largely inadequate. Markers such as serum creatinine, formulas to estimate glomerular filtration rate, cystatin C, and proteinuria largely identify an underlying disease process that is well established. Thus, there has been a recent effort to identify new biomarkers that reflect kidney function, early injury, and/or repair that ultimately can relate to progression or regression of damage. Several biomarkers emerged recently that are able to detect kidney damage earlier than is currently possible with traditional biomarkers such as serum creatinine and proteinuria. Identification of urine biomarkers has proven to be beneficial in recent years because of ease of handling, stability, and the ability to standardize the various markers to creatinine or other peptides generally already present in the urine. Recent markers such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and podocin have garnered a lot of attention. The emergence of these and other biomarkers is largely because of the evolution of novel genomic and proteomic applications in investigations of acute kidney injury and chronic kidney disease. In this article, we focus on the applications of these biomarkers in disease.

19 Review Is there a future for direct renin inhibitors? 2010

Chaudhary, Kunal / Nistala, Ravi / Whaley-Connell, Adam. ·Harry S Truman VA Medical Center, Columbia, MO 65211, USA. chaudharyk@health.missouri.edu ·Expert Opin Investig Drugs · Pubmed #20380486.

ABSTRACT: IMPORTANCE OF THE FIELD: The renin-angiotensin-aldosterone system (RAAS) is a key regulator of blood pressure (BP), as well as volume and electrolytes, in both hypertensive and normotensive individuals. Inappropriate activation of the RAAS is important in hypertension-induced cardiovascular disease (CVD) and chronic kidney disease (CKD). Renin is the rate-limiting step in the RAAS cascade, which makes direct renin inhibitors (DRIs) an attractive target for RAAS suppression and treatment of hypertension. Current regimens using either angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB) result in feedback upregulation of renin and aldosterone breakthrough, which contribute to incomplete suppression of the RAAS. Thereby, aliskiren - alone or in combination - might offer a novel therapeutic intervention to improve suppression of the RAAS, with potential to translate to improved CVD and CKD outcomes. AREAS COVERED IN THIS REVIEW: Herein, we present the current state of knowledge of DRIs in the preclinical and clinical realm and their antihypertensive efficacy in relation to cardiovascular and renal risk. Recent clinical trials (2007 - 2009) support the efficacy of aliskiren, and studies suggest the potential for improved CVD and CKD outcomes. WHAT THE READER WILL GAIN: An understanding of the mechanism of action of DRIs and a perspective of recent clinical trials. TAKE HOME MESSAGE: The DRI aliskiren is an effective antihypertensive agent that preliminary data suggests has a beneficial effect in CVD and CKD. Combination of aliskiren with an ACEi or ARB may be better tolerated than the ACEi-ARB combination. Future work is needed to further quantify aliskiren's impact on hard CVD and CKD end points.

20 Review Aldosterone: role in the cardiometabolic syndrome and resistant hypertension. 2010

Whaley-Connell, Adam / Johnson, Megan S / Sowers, James R. ·Department of Internal Medicine, University of Missouri-Columbia School of Medicine, Columbia, MO 65212, USA. ·Prog Cardiovasc Dis · Pubmed #20226958.

ABSTRACT: The prevalence of diabetes, hypertension, and cardiovascular disease (CVD) and chronic kidney disease (CKD) is increasing in concert with obesity. Insulin resistance, metabolic dyslipidemia, central obesity, albuminuria. and hypertension commonly cluster to comprise the cardiometabolic syndrome (CMS). Emerging evidence supports a shift in our understanding of the crucial role of elevated serum aldosterone in promoting insulin resistance and resistant hypertension. Aldosterone enhances tissue generation of oxygen free radicals and systemic inflammation. This increase in oxidative stress and inflammation, in turn, contributes to impaired insulin metabolic signaling, reduced endothelial-mediated vasorelaxation, and associated cardiovascular and renal structural and functional abnormalities. In this context, recent investigation indicates that hyperaldosteronism, which is often associated with obesity, contributes to impaired pancreatic beta-cell function as well as diminished skeletal muscle insulin metabolic signaling. Accumulating evidence indicates that the cardiovascular and renal abnormalities associated with insulin resistance are mediated, in part, by aldosterone's nongenomic as well as genomic signaling through the mineralocorticoid receptor (MR). In the CMS, there are increased circulating levels of glucocorticoids, which can also activate MR signaling in cardiovascular, adipose, skeletal muscle, neuronal, and liver tissue. Furthermore, there is increasing evidence that fat tissue produces a lipid soluble factor that stimulates aldosterone production from the adrenal zona glomerulosa. Recently, we have learned that MR blockade improves pancreatic insulin release, insulin-mediated glucose utilization, and endothelium-dependent vasorelaxation as well as reduces the progression of CVD and CKD. In summary, aldosterone excess exerts detrimental metabolic effects that contribute to the development of the CMS and resistant hypertension as well as CVD and CKD.

21 Review Dual renin-angiotensin system blockade in the ONTARGET study: clinically relevant risk for the kidney? 2009

Chaudhary, Kunal / Nistala, Ravi / Whaley-Connell, Adam. ·Department of Internal Medicine, Division of Nephrology and Hypertension, Harry S Truman Veterans Administration Medical Center, 800 Hospital Drive, Columbia, MO 65211, USA. chaudharyk@health.missouri.edu ·Curr Hypertens Rep · Pubmed #19737455.

ABSTRACT: Inhibition of the renin-angiotensin system contributes to reductions in proteinuria and in progression of chronic kidney disease. Indeed, monotherapy with either an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) has been shown to decrease proteinuria and slow the decline of chronic kidney disease, but incompletely. Therefore, there is increasing interest in whether combination strategies will provide more complete blockade of the renin-angiotensin system, which may translate into superior renoprotective and cardioprotective effects compared with either agent alone. There have been several reports on combination strategies. However, the recent report of the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) has received much of the attention. The renal outcomes in ONTARGET suggest that combined ACE inhibitor and ARB therapy contributes to a higher rate of adverse renal outcomes than monotherapy. Therefore, this review explores data from ONTARGET in relation to other available evidence on the use of combination therapies.

22 Review Narrative review: the emerging clinical implications of the role of aldosterone in the metabolic syndrome and resistant hypertension. 2009

Sowers, James R / Whaley-Connell, Adam / Epstein, Murray. ·University of Missouri, Columbia, Missouri, USA. ·Ann Intern Med · Pubmed #19487712.

ABSTRACT: The prevalence of obesity, diabetes, hypertension, and cardiovascular and chronic kidney disease is increasing in developed countries. Obesity, insulin resistance, and hypertension commonly cluster with other risk factors for cardiovascular and chronic kidney disease to form the metabolic syndrome. Emerging evidence supports a paradigm shift in our understanding of the renin-angiotensin-aldosterone system and in aldosterone's ability to promote insulin resistance and participate in the pathogenesis of the metabolic syndrome and resistant hypertension. Recent data suggest that excess circulating aldosterone promotes the development of both disorders by impairing insulin metabolic signaling and endothelial function, which in turn leads to insulin resistance and cardiovascular and renal structural and functional abnormalities. Indeed, hyperaldosteronism is associated with impaired pancreatic beta-cell function, skeletal muscle insulin sensitivity, and elevated production of proinflammatory adipokines from adipose tissue, which results in systemic inflammation and impaired glucose tolerance. Accumulating evidence indicates that the cardiovascular and renal abnormalities associated with insulin resistance are mediated in part by aldosterone acting on the mineralocorticoid receptor. Although we have known that mineralocorticoid receptor blockade attenuates cardiovascular and renal injury, only recently have we learned that mineralocorticoid receptor blockade improves pancreatic insulin release, insulin-mediated glucose utilization, and endothelium-dependent vasorelaxation. In summary, aldosterone excess has detrimental metabolic effects that contribute to the metabolic syndrome and endothelial dysfunction, which in turn contribute to the development of resistant hypertension as well as cardiovascular disease and chronic kidney disease.

23 Review Redox control of renal function and hypertension. 2008

Nistala, Ravi / Whaley-Connell, Adam / Sowers, James R. ·University of Missouri-Columbia School of Medicine, Department of Internal Medicine, Columbia, Missouri 65212, USA. nistalar@health.missouri.edu ·Antioxid Redox Signal · Pubmed #18821850.

ABSTRACT: Loss of redox homeostasis and formation of excessive free radicals play an important role in the pathogenesis of kidney disease and hypertension. Free radicals such as reactive oxygen species (ROS) are necessary in physiologic processes. However, loss of redox homeostasis contributes to proinflammatory and profibrotic pathways in the kidney, which in turn lead to reduced vascular compliance and proteinuria. The kidney is susceptible to the influence of various extracellular and intracellular cues, including the renin-angiotensin-aldosterone system (RAAS), hyperglycemia, lipid peroxidation, inflammatory cytokines, and growth factors. Redox control of kidney function is a dynamic process with reversible pro- and anti-free radical processes. The imbalance of redox homeostasis within the kidney is integral in hypertension and the progression of kidney disease. An emerging paradigm exists for renal redox contribution to hypertension.

24 Review Antihypertensive medications and their effects on lipid metabolism. 2008

Deshmukh, Mrunalini / Lee, Ho Won / McFarlane, Samy I / Whaley-Connell, Adam. ·Department of Medicine, Box 50, State University of New York Health Science Center at Brooklyn, Kings County Hospital Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA. mrunalini.deshmukh@downstate.edu ·Curr Diab Rep · Pubmed #18625119.

ABSTRACT: Hypertension and hyperlipidemia are interrelated and share common pathophysiologic mechanisms, such as insulin resistance and endothelial dysfunction. Accumulating evidence shows that it is important to regulate hypertension and hyperlipidemia to reduce cardiovascular risk. However, medications such as beta-blockers and thiazide diuretics, which are widely used for blood pressure regulation, are known to have several metabolic side effects. Despite deleterious effects on glucose metabolism and lipid metabolism, these medications have been proven to reduce cardiovascular risk. On the other hand, calcium channel blockers, angiotensin-converting enzyme inhibitors, and alpha-blockers have either no effect or favorable effects on the lipid profile. This review outlines the need to control hypertension, options for several antihypertensive medications, their differing effects on lipid metabolism, and the clinical implications of their effects on lipid parameters.

25 Article Metabolic Control of Blood Pressure Variability in Humans. 2016

Whaley-Connell, Adam / Sowers, James R. ·Research Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO. · Division of Nephrology and Hypertension, Department of Medicine, University of Missouri-Columbia School of Medicine, Columbia, MO. · Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri-Columbia School of Medicine, Columbia, MO. · Department of Medical Pharmacology and Physiology, University of Missouri-Columbia School of Medicine, Columbia, MO. · Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO. ·J Clin Hypertens (Greenwich) · Pubmed #26408208.

ABSTRACT: -- No abstract --

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