Intrarenal control of electrolyte excretion by angiotensin II

Hall, John E.; Guyton, Arthur C.; Trippodo, N. C.; Lohmeier, Thomas E.; McCaa, R E; Cowley, Allen W.

doi:10.1152/ajprenal.1977.232.6.f538

Cited by 60 publications

(37 citation statements)

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“…GFR and FF (GFR/RCBF) only temporarily but significantly declined and returned to or towards control values within 60 to 120 min. These results are similar to those found in normal dogs (Hall et al, 1977a) and can generally be interpreted as renal vasodilatation due to inhibition ofAII-induced vasoconstriction (Hall et al, 1977b). Furthermore, when the infusion of saralasin was stopped RCBF and calculated resistance returned to baseline values while GFR and FF increased significantly above control values, suggesting that replacement of saralasin by endogenous All at the receptor site leads to marked vasoconstriction, presumably of the efferent arterioles (Hall et al, 1977b;1981).…”

Section: Discussionsupporting

confidence: 81%

Urinary kallikrein excretion during inhibition of endogenous angiotensin II in the pig

Binder¹,

Maier²,

Rana³

et al. 1986

British J Pharmacology

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1 This study was performed to assess the possible contribution ofendogenous angiotensin II (All) to the regulation of urinary kallikrein excretion. The All antagonist saralasin or the saline vehicle was infused into the aorta above the renal arteries of pigs under halothane-02/N20 anaesthesia. Systemic and renal functional parameters were followed for 140 min and during stimulation of the reninangiotensin system by haemorrhage. 2 Urinary kallikrein excretion, determined as kininogenase activity, was increased immediately upon both initiation and termination of the 2 h saralasin infusion into pigs not subjected to haemorrhage. Renal cortical blood flow (RCBF) was maintained in both saline and saralasin-treated animals at blood pressures as low as 70 mm Hg, while glomerular filtration rate was dissociated during saralasin infusion. As long as RCBF was maintained, urinary kallikrein excretion rate was elevated during the progressive hypotension in both saline and saralasin-treated animals. 3 These findings confirm a close relationship between the maintenance of RCBF and increased activity of the kallikrein-kinin system whether or not All is antagonized, and indicate that during haemorrhage the kallikrein-kinin system is stimulated by a mechanism not involving All.

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Section: Discussionsupporting

confidence: 81%

Urinary kallikrein excretion during inhibition of endogenous angiotensin II in the pig

Binder¹,

Maier²,

Rana³

et al. 1986

British J Pharmacology

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“…Although extra-hepatic AGT is not thought to provide a source of circulating AGT, local synthesis of other components of the RAS including angiotensin II receptors in these tissues suggests the potential for both local synthesis and action of angiotensin II. Indeed, angiotensin II has been postulated to regulate blood flow, natriuresis, and tubuloglomerular feedback in the kidney (2,3) and to facilitate neurotransmission, sympathetic outflow, and arginine vasopressin release in the central nervous system (4,5). Angiotensin II may also play an important role in the development of some organs (6).…”

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confidence: 99%

Efficient Liver-specific Deletion of a Floxed Human Angiotensinogen Transgene by Adenoviral Delivery of Cre Recombinasein Vivo

Stec¹,

Davisson²,

Haskell

et al. 1999

Journal of Biological Chemistry

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Tissue-specific ablation of gene function is possible in vivo by the Cre-loxP recombinase system. We generated transgenic mice containing a human angiotensinogen gene flanked by loxP sites (hAGT flox ). To examine the physiologic consequences of tissue-specific loss of angiotensinogen gene function in vivo, we constructed an adenovirus expressing Cre recombinase. Studies were performed in several independent lines of hAGT flox mice before and after intravenous administration of either Adcre or Ad␤Gal as a control. Systemic administration of Adcre caused a significant decrease in circulating human angiotensinogen and markedly blunted the pressor response to administration of purified recombinant human renin. Southern blot analysis of genomic DNA from various organs revealed that the Cre-mediated deletion was liver-specific. Further analysis revealed the absence of full-length human angiotensinogen mRNA and protein in the liver but not the kidney of Adcre mice, consistent with the liver being the target for adenoviruses administered intravenously. These studies demonstrate that extra-hepatic sources of angiotensinogen do not contribute significantly to the circulating pool of angiotensinogen and provide proof-of-principle that the Cre-loxP system can be used effectively to examine the contribution of the systemic and tissue reninangiotensin system to normal and pathological regulation of blood pressure.

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“…2o . 63 Another observation that supports the view that the effects of ACE inhibitors are mediated mainly by blockade of angiotensin II formation is that angiotensin II infusion at physiologic rates almost completely reverses the changes in renal hemodynamics, sodium excretion, and blood pressure caused by ACE inhibitors . If endogenously produced kin ins or pro taglandins play an important role in reducing blood pressure after ACE inhibition , it seems likely that complete re toration of blood pressure by angiotensin II infusion would require a greater amount of angiotensin II than would be required to restore plasma aldosterone concentration, since kinin have not been found to reduce aldosterone secretion.…”

Section: The Specificity Of Ace Inhibitorsmentioning

confidence: 88%

Control of blood pressure by the renin‐angiotensin‐aldosterone system

Hall

1991

Clinical Cardiology

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Summary: Modification of the renin-angiotensin system, part of a powerful feedback system for long-term control of arterial pressure and volume homeostasis, through use of angiotensin-converting enzyme (ACE) inhibitors, offers a powerful means of reducing blood pressure in many hyperten ive patients . There is considerable evidence to suggest that the chronic renal and blood pressure actions of ACE inhibitors are mediated mainly by blockade of angiotensin II formation , rather than by other effects such as increased levels of kinins or prostaglandins . The loogterm actions of angiotensin U and aldosterone on blood pressure are closely intertwined with their effects on volume homeostasis and the renal pressure natriuresis mechanism. In most instances, changes in angiotensin II and aldosterone act to amplify the effectiveness of pressure natriuresis and minimize changes .in blood pressure needed to maintain sodium balance. When angiotensin II or aldosterone levels are inappropriately elevated, the antinatriuretic effects of these hormones shift pressure natriuresis to higher levels, thereby necessitating increased blood pressure to maintain sodium balance. Control of renal excretory function and modulation of pressure natriuresis by angiotensin II is mediated by intrarenal and extrarenal effects, including stimulation of aldosterone secretion. Current evidence indicates that the intra renal effects of angiotensin II are quantitatively more important than changes in aldosterone in regu lating renal excretion and arterial pressure. The intrarenal actions of angiotensin II include a direct effect on tubular sodium transport as well as a potent constrictor action on efferent arterioles , which increases reabsorption by altering peritubular capillary forces. The constrictor effect of angiotensin II on efferent arterioles also helps to stabilize glomerular filtration rate and therefore excretion of metabolic waste products, an action that may be particularly important when renal perfusion is impaired (e.g. , in renal artery stenosis or heart failure).

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Intrarenal control of electrolyte excretion by angiotensin II

Cited by 60 publications

References 0 publications

Urinary kallikrein excretion during inhibition of endogenous angiotensin II in the pig

Urinary kallikrein excretion during inhibition of endogenous angiotensin II in the pig

Efficient Liver-specific Deletion of a Floxed Human Angiotensinogen Transgene by Adenoviral Delivery of Cre Recombinasein Vivo

Control of blood pressure by the renin‐angiotensin‐aldosterone system

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