The control of renin release

Davis, James O.

doi:10.1016/0002-9343(73)90134-4

Cited by 207 publications

(58 citation statements)

References 87 publications

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“…Circulating All levels directly regulate renin release independent of any hemodynamic, neurogenic, or renal tubular mechanisms via the so-called short feedback loop (1,13). In a previous study, we demonstrated that All reduces renin release in normal sodium-restricted subjects at subpressor concentrations within the physiologic range (8).…”

Section: Discussionmentioning

confidence: 86%

“…After captopril treatment, All now produced significant declines in PRA in the hypertensives; moreover, comparing declines pre-and postcaptopril, INTRODUCTION An increased intrarenal concentration of angiotensin II (All)' reduces renin release, the so-called "short feedback loop," and is thought to be one important determinant of renin release in normal man (1)(2)(3)(4)(5)(6)(7). We have demonstrated a blunted action of AII in limiting renin release in patients with essential hypertension (8).…”

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confidence: 98%

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Abnormal Renin Short Feedback Loop in Essential Hypertension Is Reversible with Converting Enzyme Inhibition

et al. 1982

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A B S T R A C T The suppression of renin release by angiotensin II (All) (the so-called short feedback loop) is blunted in essential hypertension. To determine whether this abnormality is reversible, renin release was assessed in sodium-restricted essential hypertensives and normal controls: (a) during the administration of captopril for varying intervals and (b) following the infusion of graded doses of All (0.3-3 ng/kg per min) before and after plasma levels of AII had been chronically reduced with captopril (25-50 mg every 6 h) for 70 h.In control subjects, the maximal increment above control in plasma renin activity (PRA) after a single dose of captopril (11.9±3 ng/ml per h) was significantly (P < 0.02) greater than in hypertensives (8.1±1.7 ng/ml per h) despite similar reductions in AII levels and significantly greater decrements in diastolic blood pressure in the hypertensives. When captopril was continued for 70 h, the PRA increments above base line in hypertensive subjects (11.4±2.9 ng/ml per h) rose to levels seen in the controls (11±2.6 ng/ml per h); there were no significant differences in the AII or diastolic blood pressure decrements between the two groups.Compared with normotensive subjects, AII failed to suppress renin release in hypertensive subjects despite significantly greater diastolic blood increments and comparable All levels achieved at each All dose.After captopril treatment, All now produced significant declines in PRA in the hypertensives; moreover, comparing declines pre-and postcaptopril, This work was presented at the 63rd Annual Meeting of the Endocrine Society, Abstract 714, Cincinnati, OH.

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Section: Discussionmentioning

confidence: 86%

mentioning

confidence: 98%

Abnormal Renin Short Feedback Loop in Essential Hypertension Is Reversible with Converting Enzyme Inhibition

et al. 1982

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“…There is now much evidence that renin secretion is markedly influenced by the sympathetic nervous system and catecholamines acting on renal j-adrenoceptors (Vander, 1965;Wathen, Kingsbury, Stouder, Schneider & Rostorfer, 1965;Assaykeen, Clayton, Goldfien & Ganong, 1970;Ueda, Yasuda, Takabatake, lizuka, lizuka, Ihori & Sakamoto, 1970;Johnson, Davis & Witty, 1971;Winer, Chokshi & Walkenhorst, 1971;Ganong, 1972;Tanigawa, Allison & Assaykeen, 1972;Davis, 1973;Vandongen, Peart & Boyd, 1973). It is believed that the effect of many hormones on their target cells is mediated by stimulation of adenyl-cyclase leading to increase in 3',5' cyclic adenosine monophosphoric acid (cyclic AMP), regarded as the 'second messenger' (Robison, Butcher & Sutherland, 1971;Butcher, Robison & Sutherland, 1972).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Cyclic Adenosine 3′,5′‐monophosphate and Guanosine 3′,5′‐monophosphate and Theophylline on Renin Secretion in the Isolated Perfused Kidney of the Rat

Peart

Quesada

Tényi

1975

British J Pharmacology

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The influence of cyclic adenosine 3′,5′‐monophosphate (cyclic AMP), cyclic guanosine 3′,5′‐monophosphate (cyclic GMP) and theophylline on renin secretion was examined in the isolated kidney of the rat perfused with Krebs dextran solution. Neither cyclic AMP (10−6 to 10−4 M) nor dibutyryl cyclic AMP (10−5 M) produced an increase in renin secretion. Cyclic GMP and 8 Br‐cyclic GMP caused a small rise in renin secretion in some experiments but this effect was independent of the dose and its physiological significance is uncertain. Theophylline (10−6 to 10−4 M) caused a significant elevation in renin secretion which was not blocked by (+)‐propranolol. Theophylline with cyclic AMP or cyclic GMP did not produce an amplified effect. Despite previous suggestions that cyclic AMP stimulated renin secretion, this could not be confirmed in the present preparation. Since there is no evidence that cyclic AMP or cyclic GMP (or their derivatives, dibutyryl cyclic AMP and 8 Br‐cyclic GMP) enter the cells, it will be necessary to study their activity in isolated juxtaglomerular cells to define a possible rǒle.

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“…that part of the intravenously infused catecholamine did not reach the synaptic cleft, and the pressor response to norepinephrine may have attenuated betareceptor-mediated renin stimulation by activating the renal baroreceptors. 31 It appears possible that renin-norepinephrine interrelationships in the chronic state may differ from those under acute conditions. Certain reports of a close positive correlation between plasma renin and norepinephrine or total catecholamine levels in essential hypertension 8 -• could not be confirmed by other investigators.…”

Section: Discussionmentioning

confidence: 99%

Effects of short-term norepinephrine infusion on plasma catecholamines, renin, and aldosterone in normal and hypertensive man.

Beretta-Piccoli¹,

Weidmann²,

Meier³

et al. 1980

Hypertension

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SUMMARYThe acute responsiveness of plasma catecbolamine, renln (PRA), and aldosterone levels to exogenous norepinephrine was studied under placebo conditions and following renin-angiotensin activation by diuretic pretreatment in 25 normal subjects and 34 patients with borderllne-to-moderate essential hypertension. Norepinephrine infusion caused increases in plasma norepinephrine (PNE) that correlated with the infused norepinephrine dose (p < 0.001); this relationship was similar in normal and hypertensive subjects and unaltered by diuretic therapy. Plasma eplnephrine and dopamine levels were unchanged during norepinephrine infusion. Norepinephrine infusion at pressor doses stimulated PRA (p < 0.01). The PRA responses correlated with the dose of infused norepinephrine [p < 0.0025), and norepinephrlne-stimolated PRA correlated with basal PRA (p < 0.001). These norepinephrine-PRA relationships were unaltered by diuretic treatment and similar in normal and hypertensive subjects. In both groups, norepinephrine also caused a similar Increase in plasma aldosterone (p < 0.05) under placebo conditions, but not following diuretic therapy. These findings demonstrate that an acute increase in the blood levels of the adrenergic neurotransmittor, norepinephrine, causes mild but distinct stimulation of plasma renin and aldosterone levels. Renin release in response to exogenous norepinephrine is not enhanced following renin-angiotensin activation by diuretic pretreatment. The responsiveness of the renin-angiotensin-aldosterone system to an acute norepinephrine input seems to be intact in essential hypertension.

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The control of renin release

Cited by 207 publications

References 87 publications

Abnormal Renin Short Feedback Loop in Essential Hypertension Is Reversible with Converting Enzyme Inhibition

Abnormal Renin Short Feedback Loop in Essential Hypertension Is Reversible with Converting Enzyme Inhibition

The Effects of Cyclic Adenosine 3′,5′‐monophosphate and Guanosine 3′,5′‐monophosphate and Theophylline on Renin Secretion in the Isolated Perfused Kidney of the Rat

Effects of short-term norepinephrine infusion on plasma catecholamines, renin, and aldosterone in normal and hypertensive man.

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