Angiotensin Ii Blood-Levels in Human Hypertension

Catt, K. J.; Zimmet, Paul; Cain, Michael D.; Cran, E.; Best, John; Jp, Coghlan

doi:10.1016/s0140-6736(71)91085-3

Cited by 110 publications

(53 citation statements)

References 27 publications

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“…Thus, administration of aminoglutethimide to patients with normal renin essential hypertension decreases their aldosterone production, and presumably their blood volume (8,27), but the rapid rise in renin and angiotensin II concentrations would be expected to lead to vasoconstriction, thereby compensating in part for the tendency towards reduced blood pressure secondary to the decrease in blood volume. In contrast, patients with low renin essential hypertension have low plasma concentrations of angiotensin 11 (34,35), and may be more dependent upon blood volume for maintenance of blood pressure. Thus, their hypertension might be expected to respond more readily to the antialdosterone actions of aminoglutethimide.…”

Section: Methodsmentioning

confidence: 99%

Effect of Aminoglutethimide on Blood Pressure and Steroid Secretion in Patients with Low Renin Essential Hypertension

et al. 1978

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A B S T R A C T An inhibitor of adrenal steroid biosynthesis, aminoglutethimide, was administered to seven patients with low renin essential hypertension, and the antihypertensive action of the drug was compared with its effects on adrenal steroid production. In all patients aldosterone concentrations in plasma and urine were within normal limits before the study. Mean The gradual lowering of blood pressure and body weight during aminoglutethimide therapy is consistent with the view that the antihypertensive effect of the drug is mediated through a reduction in the patients' extracellular fluid volume, probably secondary to the persistent decrease in aldosterone production. The observation that chronic administration of aminoglutethimide lowered blood pressure in these patients and elevated their plasma renin activity to the normal range without decreasing production of the adrenal steroids, deoxycorticosterone, 18-hydroxydeoxycorticosterone, and 16,3-hydroxydehydroepiandrosterone, makes it unlikely that these steroids are responsible either for the decreased renin or the elevated blood pressure in patients with low renin essential hypertension.

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Section: Methodsmentioning

confidence: 99%

Effect of Aminoglutethimide on Blood Pressure and Steroid Secretion in Patients with Low Renin Essential Hypertension

et al. 1978

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“…The activity of both the systemic and tissue RAS in hypertension is upregulated in many patients with primary hypertension. 66 Ang II can directly modulate blood pressure via activation of AT1-R in vascular smooth muscle cells and the kidney, thus causing vasoconstriction and sodium and water retention. AT1-R has also been identified in several other tissues (for example, heart and central nervous system) and may also indirectly modulate blood pressure.…”

Section: 65mentioning

confidence: 99%

The sympathetic nervous system and blood pressure in humans: implications for hypertension

2011

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A neurogenic component to primary hypertension (hypertension) is now well established. Along with raised vasomotor tone and increased cardiac output, the chronic activation of the sympathetic nervous system in hypertension has a diverse range of pathophysiological consequences independent of any increase in blood pressure. This review provides a perspective on the actions and interactions of angiotensin II, inflammation and vascular dysfunction/brain hypoperfusion in the pathogenesis and progression of neurogenic hypertension. The optimisation of current treatment strategies and the exciting recent developments in the therapeutic targeting of the sympathetic nervous system to control hypertension (for example, catheter-based renal denervation and carotid baroreceptor stimulation) will be outlined. Keywords: sympathetic nerve activity; neurogenic hypertension; immune-to-brain signalling The sympathetic renaissancePrimary (or essential) hypertension (termed hypertension from here on) accounts for the vast majority of hypertensive cases (B95%).1 Although the aetiology of this condition is incompletely understood, it appears that along with genetic factors, several environmental and behavioural 'hypertensiogenic' factors have been identified, such as obesity, insulin resistance, high-salt intake, low physical activity levels and stress.1 Given the elevated risk of stroke, renal failure, myocardial infarction and coronary heart disease in those afflicted with high blood pressure, the elucidation of the key pathogenic features and optimisation of effective therapeutic strategies are critical.The most common form of hypertension is neurogenic hypertension, defined as high blood pressure with sympathetic overdrive, loss of parasympathetically mediated cardiac variability and excessive angiotensin II (Ang II) activity.2 The importance of the sympathetic nervous system in the short-term regulation of blood pressure via the modulation of peripheral vascular tone and cardiac output is well established, while the role of the sympathetic nerve activity (SNA) in long-term blood pressure control is more controversial. [3][4][5] Although the concept of a potential neurogenic component to hypertension is not new, 4 it has perhaps received less attention than the renin-angiotensin system (RAS), which has been a prominent therapeutic and research target in hypertension over the past few decades. Nevertheless, the activation of the sympathetic nervous system and the RAS in hypertension appears inextricably, and reciprocally, linked. Evidence from studies in both patients and animal models of hypertension strongly implicate the chronic sympathetic neural activation in the aetiology and progression of hypertension (Figure 1). 2,[6][7][8][9] The use of regional surgical sympathectomy to treat hypertension over 50 years ago before the availability of antihypertensive medications that lower sympathetic activity provides an early indication of the clinical appreciation for a significant neurogenic component to hypertension.10 Recent clini...

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“…At the present time, the prevailing view holds that the circulating RAS is primarily an endocrine system designed for the general mediation, through the systemic circulation, of the effects of renin on angiotensin production in plasma (12,13). This concept can be summarized as follows: renin released by the kidney circulates in plasma, where it cleaves angiotensinogen to generate angiotensin I (Al).…”

Section: Circulating Rasmentioning

confidence: 99%

“…Thus, this revised concept predicts that plasma levels of angiotensin largely represent a spillover from the tissue sites of production (15). That plasma angiotensins predominantly result from the action of kidney-derived renin on plasma (liver-derived) angiotensinogen is shown by the fall in plasma angiotensin levels that follows nephrectomy (16)(17)(18)(19), and by the hypotensive effect of anti-angiotensinogen antibodies when injected into either sodium-replete or sodium-deplete rats (20). Given this local production ofAl and All by the circulating RAS, it is apparent that such local production may be subject to tissue-specific mechanisms of regulation, which cause changes in local All concentration that are not reflected in the plasma concentrations of renin or All.…”

mentioning

confidence: 99%

Circulating and tissue angiotensin systems.

Campbell¹

1987

J. Clin. Invest.

565

167

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Angiotensin has many different actions, most of which relate, either directly or indirectly, to the regulation of blood pressure, fluid, and electrolyte homeostasis (1, 2). In addition to potent vasoconstrictor effects, actions ofangiotensin on vasculature include the stimulation ofprostaglandin release (3), the modulation of angiotensin receptor number (4), and the stimulation of angiogenesis (5). Angiotensin also has important actions on the central and peripheral nervous systems, the adrenal, kidney, intestine, and heart (6-1 1). Given these multiple diverse actions of angiotensin, two important questions are (a) which of these actions represent normal physiological events, and (b) whether such actions may assume a pathogenic role. These questions have recently been placed in sharper focus by the clinical application of inhibitors of the renin-angiotensin system (RAS),' and in particular, the use of converting enzyme inhibitors (CEIs) for the treatment of hypertension. Any attempt to answer these questions requires an accurate concept ofthe RAS. The purpose ofthis review is to discuss new concepts concerning angiotensin production by the circulating RAS, how these relate to angiotensin production within tissues, and the possible mechanisms by which CEIs lower blood pressure. The study of tissue angiotensin systems is still at an early stage. In this review I have attempted to synthesize a coherent model of the interaction between the circulating and tissue angiotensin systems, which might assist in the interpretation of new developments in this area. Circulating RASAt the present time, the prevailing view holds that the circulating RAS is primarily an endocrine system designed for the general mediation, through the systemic circulation, of the effects of renin on angiotensin production in plasma (12,13). This concept can be summarized as follows: renin released by the kidney circulates in plasma, where it cleaves angiotensinogen to generate angiotensin I (Al).

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Angiotensin Ii Blood-Levels in Human Hypertension

Cited by 110 publications

References 27 publications

Effect of Aminoglutethimide on Blood Pressure and Steroid Secretion in Patients with Low Renin Essential Hypertension

Effect of Aminoglutethimide on Blood Pressure and Steroid Secretion in Patients with Low Renin Essential Hypertension

The sympathetic nervous system and blood pressure in humans: implications for hypertension

Circulating and tissue angiotensin systems.

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