Aldosterone Antagonism Attenuates Obesity-Induced Hypertension and Glomerular Hyperfiltration

Paula, Rogério Baumgratz de; Silva, Alexandre A. da; Hall, John E.

doi:10.1161/01.hyp.0000105624.68174.00

Cited by 184 publications

(111 citation statements)

References 35 publications

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“…In this study in the Tuzla municipality, mostly a high renin level was recorded in dogs with mild, moderate, or severe hypertension. Similar results were obtained in studies in the United States (16). Renin is secreted from the kidneys when sympathetic activity is increased (2).…”

Section: Discussionsupporting

confidence: 83%

Comparison of the role of the renin-angiotensin aldosterone system in the genesis of hypertension between two groups of nonhunting dogs and hunting dogs

Jurida¹,

Ferizbegović²,

Krčmar³

2017

Turk J Vet Anim Sci

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The role of the renin-angiotensin aldosterone system in the genesis of hypertension between nonhunting dogs and hunting dogs of various breeds was comparatively studied in the city of Tuzla (Bosnia and Herzegovina). Sixty dogs were divided into four subgroups based on different age categories. Hypertension was recorded in 21 dogs or in 35% of examined dogs. Fourteen dogs had mild (23.3%), 5 dogs had moderate (8.3%), and 2 dogs had severe hypertension (3.3%). The most cases of hypertension (n = 9) were recorded in hunting dogs aged from 9 to 12 years. In subgroups of nonhunting and hunting dogs aged from 1 to 3 years, a high correlation was recorded between systolic and diastolic pressures (P < 0.0001). A certain degree of correlation was recorded between systolic pressure and renin (P = 0.037) and between heart rate and renin (P = 0.024). In subgroups of nonhunting and hunting dogs aged from 9 to 12 years, a high correlation was recorded between systolic and diastolic pressures (P = 0.006) and between diastolic pressure and heart rate (P = 0.002). A certain degree of correlation existed between systolic pressure and heart rate (P = 0.041), systolic pressure and aldosterone (P = 0.035), and heart rate and renin (P = 0.038). Increased values of renin were mostly recorded in dogs with hypertension. This research indicates the importance of routine blood pressure measurement during every examination, which can thus serve as a screening for undertaking further steps in processing the patient.

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Section: Discussionsupporting

confidence: 83%

Comparison of the role of the renin-angiotensin aldosterone system in the genesis of hypertension between two groups of nonhunting dogs and hunting dogs

Jurida¹,

Ferizbegović²,

Krčmar³

2017

Turk J Vet Anim Sci

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“…The occurrence of escape is associated with a proportional increase in GFR and renal plasma flow by approximately 20% (15). It is interesting that a role for aldosterone as a mediator of relative or absolute hyperfiltration has been suggested in other experimental settings, including dietinduced obesity, where administration of the aldosterone antagonist eplerenone markedly attenuated glomerular hyperfiltration (18).…”

Section: Discussionmentioning

confidence: 99%

Relative Glomerular Hyperfiltration in Primary Aldosteronism

Ribstein¹,

Cailar²,

Fesler³

et al. 2005

Journal of the American Society of Nephrology

182

172

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Experimental and clinical data suggest that primary aldosteronism (PA) may be associated with cardiovascular hypertrophy and fibrosis, in part independent of the BP level. Whether PA may also result in specific deleterious effects on the kidneys was less studied. In 25 patients with tumoral PA, renal studies (urinary excretion of proteins, GFR, and effective renal plasma flow [ERPF], as clearances of technetium-labeled diethylene triaminopentaacetic acid and 131 I-ortho iodohippurate, respectively) were performed both before and 6 mo after surgical cure. A control group consisting of patients with essential hypertension (EH) was studied before and after 6 mo of antihypertensive therapy. At baseline, PA and EH patients were similar with respect to demographic data, duration and level of hypertension, and GFR and ERPF. Urinary excretion of albumin and ␤2 microglobulin were higher in PA than EH (88 ؎ 26 versus 39 ؎ 12 and 0.91 ؎ 0.23 versus 0.26 ؎ 0.19 mg/24 h, respectively; both P < 0.05). Adrenalectomy was followed by a decrease in arterial BP (by 28 ؎ 3/13 ؎ 2 mmHg), urinary excretion of albumin and ␤2 microglobulin (by 48 ؎ 19 and 0.53 ؎ 0.21 mg/24 h, respectively), and GFR and ERPF (by 15 ؎ 3 and 54 ؎ 15 ml/min per 1.73 m 2 , respectively). In EH, a similar decrease in pressure was associated with a decrease in albuminuria but no change in GFR or ERPF. In 17 of the 25 PA patients who received a 6-mo treatment of spironolactone, both GFR and ERPF decreased in parallel with BP, similar to what was observed after surgery. These data suggest that PA was associated with relative hyperfiltration, unmasked after suppression of aldosterone excess.J P rimary aldosteronism (PA) is a possibly common form of endocrine hypertension in which aldosterone production is inappropriate and at least partially autonomous with regard to physiologic control by angiotensin. In recent years, the widespread use of the plasma aldosterone/ renin ratio as a screening test for PA has led to a marked increase in the proportion of hypertensive patients identified as such (1). Whether the diagnostic workup of aldosterone-producing adenomas is cost-effective regarding the potential for curability or effective protection of target organs by specific treatment remains controversial (2). Several experimental and, to a lesser extent, clinical studies suggest that long-term exposure to increased aldosterone levels may result in renal as well as cardiac and vascular toxicity that is in part independent of the BP level (3,4). Target organ damage, as assessed by the measurement of left ventricular mass or urinary excretion of albumin, may be inappropriately high with respect to the BP level in patients with PA (5,6). However, the relationship between albuminuria and renal function parameters is not clear. Specifically, it is not known whether PA-associated albuminuria may relate to a state of hyperfiltration suggested in a study in which GFR was assessed by the measurement of creatinine clearance (7). For investigating the effect of aldosterone excess...

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“…41 The involvement of aldosterone in obesity-associated hypertension was demonstrated by blockade of mineralocorticoid receptors with the specific antagonist eplerenone, which inhibited development of high blood pressure in the high-fat-fed dogs without affecting the weight gain of these animals. 42 These results indicate that aldosterone may play a significant role in development of obesity-hypertension. Aldosterone can raise blood pressure in obesity through an action on mineralocorticoid receptors located in different tissues, including the kidney, vasculature, and brain ( Figure 2).…”

mentioning

confidence: 86%

Obesity-Associated Hypertension

et al. 2005

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Abstract-Obesity is strongly associated with hypertension and cardiovascular disease. Several central and peripheral abnormalities that can explain the development or maintenance of high arterial pressure in obesity have been identified. These include activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Obesity is also associated with endothelial dysfunction and renal functional abnormalities that may play a role in the development of hypertension. The continuing discovery of mechanisms regulating appetite and metabolism is likely to lead to new therapies for obesity-induced hypertension. Better understanding of leptin signaling in the hypothalamus and the mechanisms of leptin resistance should facilitate therapeutic approaches to reverse the phenomenon of selective leptin resistance. Other hunger and satiety signals such as ghrelin and peptide YY are potentially attractive therapeutic strategies for treatment of obesity and its complications. These recent discoveries should lead to novel strategies for treatment of obesity and hypertension. (Hypertension. 2005;45:9-14.)Key Words: hypertension, obesity Ⅲ nervous system, sympathetic renal Ⅲ vasculature Ⅲ kidney T he increasing prevalence of obesity worldwide is a serious health hazard. This is particularly true for the United States, where Ϸ300 000 deaths each year are associated with being overweight and obese. Obese individuals are at increased risk for diabetes, hypertension, renal failure, and other cardiovascular diseases. Clinical and animal studies have confirmed a strong relationship between obesity and hypertension. 1 Accumulating evidence points to visceral obesity as the most important risk factor for hypertension and cardiovascular disease. 2 Recent work has identified several mechanisms that have therapeutic implications as potential causes of obesity-hypertension. In addition, to these advances, there has also been a revolution in our understanding of neuroendocrine mechanisms regulating appetite, metabolism, and adiposity since the discovery of leptin just Ͼ10 years ago. If, as we predict, these advances soon translate into safe and effective pharmacological treatment of obesity, this would also greatly impact the management of obesityhypertension. Consequently, we briefly review some highlights on advances in understanding the pathophysiology of obesity in addition to highlights on obesity-induced hypertension. New Developments in Neurobiology of ObesityThe identification of leptin represents the most significant breakthrough in obesity research because it helped unravel the architecture of neuroendocrine circuitry that controls appetite and energy homeostasis. Leptin is an adipocyte-derived hormone that acts in the hypothalamus to regulate appetite and energy expenditure. Recently, increasing attention has been dedicated to leptin transduction mechanisms (Figure 1). The leptin receptor is a single transmembrane protein belonging to the cytokine-receptor superfamily known to signal via the janus kinase/signal ...

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Aldosterone Antagonism Attenuates Obesity-Induced Hypertension and Glomerular Hyperfiltration

Cited by 184 publications

References 35 publications

Comparison of the role of the renin-angiotensin aldosterone system in the genesis of hypertension between two groups of nonhunting dogs and hunting dogs

Comparison of the role of the renin-angiotensin aldosterone system in the genesis of hypertension between two groups of nonhunting dogs and hunting dogs

Relative Glomerular Hyperfiltration in Primary Aldosteronism

Obesity-Associated Hypertension

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