Angiotensin antagonists with increased specificity for the renal vasculature.

Taub, Ken; Caldicott, William J.H.; Hollenberg, Norman K.

doi:10.1172/jci108668

Cited by 35 publications

(6 citation statements)

References 20 publications

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“…Since this would more than compensate for the hypotensive effect that resulted from removal of A II from plasma, blood pressure would rise above the control level. This explanation supports the concept of intrarenal production of A II as one component of an intrarenal renin-angiotensin system (Levens, Peach & Carey, 1981;Mendelsohn, 1982 (Peach, 1977 (Freeman, Davis & Lohmeier, 1975;Taub, Caldicott & Hollenberg, 1977;Caldicott, Taub, Margulies & Hollenberg, 1981). Other investigators however have reported that in the dog, A II is a more potent renal vasconstrictor than A III and demonstrated that this was not due to differential release of prostaglandins (Satoh, Itsukaichi, Ohyama & Hayashi, 1981).…”

Section: Discussionsupporting

confidence: 63%

“…achieved steady states during the CEI + angiotensin periods in Groups 1 and 2 with the same dose of each peptide. Previous studies in the dog have compared the renal actions of A II and A III and, in most cases, have shown that in contrast to the systemic pressor action, the two peptides are equipotent in their actions in the renal vasculature (Freeman, Davis & Lohmeier, 1975;Taub, Caldicott & Hollenberg, 1977;Caldicott, Taub, Margulies & Hollenberg, 1981). Other investigators however have reported that in the dog, A II is a more potent renal vasconstrictor than A III and demonstrated that this was not due to differential release of prostaglandins (Satoh, Itsukaichi, Ohyama & Hayashi, 1981).…”

Section: Discussionmentioning

confidence: 99%

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Reversal by angiotensins II and III of the effects of converting enzyme inhibition on renal electrolyte excretion in rats.

Harris¹,

Munro²

1984

The Journal of Physiology

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SUMMARY1. Experiments were carried out in anaesthetized rats to compare the abilities of angiotensin II (A II) and angiotensin III (A III) to reverse the effects of angiotensin converting enzyme inhibition (Teprotide) on salt and water excretion.2. In rats infused with Teprotide, significant increases in urine flow and sodium excretion were observed and arterial blood pressure decreased. Addition of A II (10 pmol min-) to the Teprotide infusion reduced renal excretion of sodium and water to control values and excretion of potassium to below control. Blood pressure increased to a value significantly higher than that during the control period.3. In a separate group of rats the natriuretic and diuretic effects of Teprotide were reversed by a similar dose ofA III (10 pmol min-'). A primarily angiotensin-mediated action is indicated for the renal effects of Teprotide.4. Although angiotensins II and III appeared to be equipotent in their abilities to reverse the renal responses to Teprotide, A II caused an increase in arterial blood pressure that was not seen with A III. In a third group of rats A II (10 pmol min-) was added to the Teprotide infusion and an aortic snare located between the renal arteries was tightened to prevent any increase in left renal perfusion pressure. During this period the rate of sodium excretion from the left kidney was significantly lower than from the right kidney.5. It is concluded that in the absence of any accompanying 'pressure natriuresis' A II is more potent than A III in its ability to reverse the natriuretic action of Teprotide. The elevation of blood pressure to above control values by a dose of A II only just sufficient to reverse the Teprotide-induced natriuresis suggests that the concentration of angiotensin in the kidney is higher than in plasma and supports the concept of an intrarenal renin-angiotensin system. 6. In the rat both A II and A III may affect renal salt and water excretion by a combination of mechanisms involving glomerular, vascular and tubular receptors. The possibility is raised that differential effects of the active angiotensins on these mechanisms may participate in the regulation of sodium excretion.

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Section: Discussionsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Reversal by angiotensins II and III of the effects of converting enzyme inhibition on renal electrolyte excretion in rats.

Harris¹,

Munro²

1984

The Journal of Physiology

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“…Recently, however, Freeman et al (1975) infused both angiotensins II and III ([des-Asp']-angiotensin II) into the renal artery of sodium-replete dogs and noted comparable reductions in renal blood flow and renin release in response to both compounds. In contrast, Taub et al (1977) showed angiotensin II to have a greater effect on the renal vasculature than angiotensin III. Furthermore, in Taub's studies, crosstachyphylaxis between the peptides occurred, which led to the assumption that angiotensins II and III act in the kidney on a single receptor which has structural properties that differ from those of the systemic vascular angiotensin receptor.…”

Section: Intrarenal Role Of Angiotensin IIImentioning

confidence: 88%

Role of the intrarenal renin-angiotensin system in the control of renal function.

Levens¹,

Peach²,

Carey³

1981

Circulation Research

178

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IN THIS review article, we will assess the evidence for the presence and the mechanism of the intrarenal renin-angiotensin system acting as a local hormonal system in the control of renal function. First, we will review the evidence for the presence of a renin-angiotensin system in the kidney. Second, using results of our own and other studies, we will develop the concept that the intrarenal renin-angiotensin system acts as a local hormonal system in the control of renal function. Third, we will discuss experimental observations on the intrarenal effects of angiotensin II. Fourth, we will evaluate the evidence for a direct renal tubular action of angiotensin II. Fifth, we will assess the role of the intrarenal renin-angiotensin system in renal autoregulation. Finally, we will speculate on the function of the intrarenal renin-angiotensin system in the regulation of fluid and electrolyte homeostasis in general.

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“…Because the pressor activity of intravenously administered angiotensin III is approximately 20-30% of the activity of angiotensin II (Carey et al, 1978), angiotensin III may be expected to be a less potent vasoconstrictor in the major peripheral vasculatures. Angiotensin II and angiotensin III, however, have been reported to have equal vasoconstrictor effects in the renal (Freeman et al, 1975;Taub et al, 1977) and in the mesenteric and femoral vasculatures . This finding indicates that mechanisms associated with differential responses in mesenteric blood flow to angiotensin II and angiotensin III are not involved in the contrasting responses in arterial pressure elicited by these compounds.…”

mentioning

confidence: 99%

A comparison of angiotensin II and angiotensin III as vasoconstrictors in the mesenteric circulation of dogs.

Britton¹,

Sexton²,

Fiksen-Olsen³

et al. 1980

Circulation Research

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Angiotensin II is more potent as a vasopressor than angiotensin III when given intravenously. We tested the hypothesis that differential changes in mesenteric blood flow contribute to this difference in potency. The effects of angiotensin II and angiotensin III on mesenteric blood flow were compared in 31 dogs anesthetized with pentobarbital. These agonists were administered either as bolus injections (10-160 pmol) or as constant infusions (30 pmol/min per kg) directly into the vasculature supplied by the superior mesenteric artery. Approximately equipressor doses of angiotensin II (40 pmol/min per kg) and angiotensin III (80 pmol/min per kg) also were given intravenously. On the basis of duration and graphic integration of the response in mesenteric blood flow, but not on the basis of absolute change in amplitude, angiotensin II was consistently more potent than angiotensin III as a mesenteric vasoconstrictor. The intra-arterial and intravenous constant infusion doses were repeated after the administration of meclofenamate (4 mg/kg, iv). Meclofenamate did not alter any of the responses to angiotensin II or angiotensin III. We conclude that the differential constrictor properties of these compounds in the mesenteric vasculature contribute to the greater potency of intravenously administered angiotensin II on arterial pressure. The results provide no evidence for an interaction between prostaglandins and the vasoconstrictor properties of angiotensin II or III in the intact mesenteric vasculature of the anesthetized dog. Circ Res 46:146-151, 1980

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Angiotensin antagonists with increased specificity for the renal vasculature.

Cited by 35 publications

References 20 publications

Reversal by angiotensins II and III of the effects of converting enzyme inhibition on renal electrolyte excretion in rats.

Reversal by angiotensins II and III of the effects of converting enzyme inhibition on renal electrolyte excretion in rats.

Role of the intrarenal renin-angiotensin system in the control of renal function.

A comparison of angiotensin II and angiotensin III as vasoconstrictors in the mesenteric circulation of dogs.

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