Neuroendocrine components in the regulation of blood pressure and renin secretion.

Ganong, William F.; Rudolph, Colin D.; Zimmermann, Heinz

doi:10.1161/01.hyp.1.3.207

Cited by 54 publications

(37 citation statements)

References 81 publications

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“…After i.v.t. testing, argininevasopressin (Parke-Davis) (1,10,25,50, and 100 mU/kg) was injected i.v. in a volume of 0.5 ml/kg.…”

Section: Test Procedures Blood Pressure Responsementioning

confidence: 99%

“…The central pressor effect of All is blunted in sodium-depleted rats. To assess the specificity of the sodium effect on All, central cholinergic neurons, which may also be implicated in central BP regulation, 1 were stimulated. Carbachol, administered centrally, elicited BP increases that were about equal to those observed with All, but which were not affected by low sodium intake.…”

Section: Blood Pressurementioning

confidence: 99%

See 1 more Smart Citation

Central actions and brain receptor binding of angiotensin II: Influence of sodium intake.

Mann¹,

Schiffrin²,

Schiller³

et al. 1980

Hypertension

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“…After i.v.t. testing, argininevasopressin (Parke-Davis) (1,10,25,50, and 100 mU/kg) was injected i.v. in a volume of 0.5 ml/kg.…”

Section: Test Procedures Blood Pressure Responsementioning

confidence: 99%

Section: Blood Pressurementioning

confidence: 99%

Central actions and brain receptor binding of angiotensin II: Influence of sodium intake.

Mann¹,

Schiffrin²,

Schiller³

et al. 1980

Hypertension

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“…In addition to activation of the hypothalamicpituitary-adrenal axis and the sympathoadrenal system, which are the major neuroendocrine components of the acute stress response (1)(2)(3)(4), most physical-psychologic stress paradigms ity (PRA)' and plasma aldosterone levels (5)(6)(7)(8)(9)(10) . PRA is elevated after immobilization, handling, and head-up tilt in rats, and arithmetic or intelligence quotient tests in humans (5)(6)(7)(8)(9)(10). The mechanism by which PRA increases in response to acute stress involves sympathetic activation, since the increases are attenuated by renal denervation and ,3-adrenergic blockers (5,11,12).…”

Section: Introductionmentioning

confidence: 99%

Hyperreninemic hypoaldosteronism after chronic stress in the rat.

Aguilera¹,

Kiss²,

Sunar-Akbasak³

1995

J. Clin. Invest.

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The effects of chronic stress on the renin-angiotensin-aldosterone system were studied by analysis of plasma hormone levels, kidney renin mRNA levels, adrenal angiotensin II receptors, and steroidogenesis in rats subjected to repeated immobilization (2 h daily) or intraperitoneal injections of 1.5 M NaCl for 14 d. 24 h after the last stress in both stress models, plasma aldosterone levels were reduced in spite of significant increases in plasma renin activity. Repeatedly intraperitoneal hypertonic saline-injected rats showed plasma renin activity responses to acute immobilization similar to controls, but markedly reduced plasma aldosterone responses. Concomitant with the increases in plasma renin activity, renin mRNA levels in the kidney were significantly increased in intraperitoneal hypertonic saline-injected rats, and these increases were prevented by ,B-adrenergic receptor blockade with propranolol. In isolated adrenal glomerulosa cells from chronically stressed rats, maximum aldosterone responses to angiotensin II, ACTH, and 8-Br-cAMP were significantly decreased, whereas pregnenolone responses were increased. P450-aldosterone synthetase mRNA levels and binding of '"I-[Sar',Ile8]angiotensin II were significantly reduced in the adrenal zona glomerulosa of stressed rats. These studies show that chronic repeated stress leads to renin stimulation due to sympathetic activation, and inhibition of aldosterone secretion due to inhibition of the late steroidogenic pathway. The data provide evidence for a role of chronic stress in the development of hyperreninemic hypoaldosteronism. (J. Clin. Invest. 1995. 96:1512-1519

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“…Renin, as distinct from acid protease, 5 has been extracted from brain tissue of rats,' dogs, 7 and humans; 8 renin substrate has been extracted from dog brain and partially purified; 9 converting enzyme has been extracted from rat brain, 10 localized and partially purified; 11 angioJtensin-like peptides have been demonstrated to be present in cerebrospinal fluid and brain tissue,"- 13 and specific high affinity binding sites for angiotensin II are present in brain tissue. This system has been suggested to play a role in the maintenance of blood pressure (BP) in the spontaneous hypertensive rat since intracerebroventricular administration of competitive antagonists of angiotensin II lowered BP in six of seven recent reports.…”

Section: T He Possible Existence Of An Independentmentioning

confidence: 99%

Blood pressure responses of conscious normotensive and spontaneously hypertensive rats to intracerebroventricular and peripheral administration of captopril.

Hutchinson¹,

Mendelsohn²,

Doyle³

1980

Hypertension

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SUMMARYIn conscious spontaneously hypertensive rats, intracerebroTentricular injection of captopril (2 rag/kg) resulted in a rapid hypotenshe response that lasted several hours. The same dose given by Intracerebroventricular injection had no significant effect on blood pressure (BP) of normotensive Wistar-Kyoto (WK) rats over 7 hours. There was no significant change in BP of conscious spontaneously hypertensive rats (SHR) in response to Intracerebroventricular injection of vehicle and only a transitory fall in BP in response to intravenous injection of captopril (2 mg/kg). There was no significant differences between plasma renin activity (PRA) of conscious norrootenslve WKY rats and the PRA of SHR. These results suggest biochemical differences between the brains of SHR and normotensive WKY control rats. These differences could involve the brain renin-angiotensin system or other iteuropeptides. renin-angiotensin system in the brain has been the subject of some controversy.

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Neuroendocrine components in the regulation of blood pressure and renin secretion.

Cited by 54 publications

References 81 publications

Central actions and brain receptor binding of angiotensin II: Influence of sodium intake.

Central actions and brain receptor binding of angiotensin II: Influence of sodium intake.

Hyperreninemic hypoaldosteronism after chronic stress in the rat.

Blood pressure responses of conscious normotensive and spontaneously hypertensive rats to intracerebroventricular and peripheral administration of captopril.

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