The renin-angiotensin system

Peart, W. S.

doi:10.1007/978-1-349-02718-7_10

Cited by 89 publications

(25 citation statements)

References 73 publications

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“…Sodium depletion was produced in the present experiments by a low sodium intake and by administration of furosemide (1,17,33). Hypovolemia probably was responsible for the reduced cardiac output and left ventricular end-diastolic pressure in these sodium-depleted dogs.…”

Section: Discussionmentioning

confidence: 50%

“…Saralasin is a competitive receptor antagonist of angiotensin II (4,12,13), whereas the latter two agents inhibit angiotensin-converting enzyme, which converts angiotensin I to the biologically active angiotensin II (8,(13)(14)(15)(16). Because angiotensin II is one of the most potent vasoconstrictors known (17,18), a decrease in arterial blood pressure after angiotensin inhibition presumably is due to elimination of the angiotensin-induced vasoconstriction. However, angiotensin II also exerts a positive inotropic action on the heart (19,20), the abolition of which may lower the arterial pressure.…”

Section: Introductionmentioning

confidence: 99%

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Renin-Angiotensin System Inhibition in Conscious Sodium-Depleted Dogs

Liang¹,

Gavras²,

Hood³

1978

J. Clin. Invest.

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A B S T R A C T The role of the renin-angiotensin system in the regulation of the systemic and coronary circulations during sodium depletion was studied in conscious normotensive dogs by i.v. administration of teprotide (0.5 mg/kg), an angiotensin-converting enzyme inhibitor, and saralasin (0.05-5 ,ug/kg per min), an angiotensin-receptor antagonist. Sodium depletion was produced by administering a low sodium diet and furosemide for 5 days. Administration of both teprotide and saralasin lowered systemic arterial blood pressure and total peripheral vascular resistance. Simultaneously, cardiac output increased, but left ventricular end-diastolic pressure, dP/dt, and dP/dt/P did not change significantly. Furthermore, both agents reduced diastolic coronary vascular resistance and increased coronary blood flow, but did not affect myocardial oxygen consumption, left ventricular work, or myocardial efficiency. These systemic and coronary vasodilator effects of teprotide and saralasin, however, were not observed in normal dogs on a regular sodium diet; in this group, the only effect noted was a slight increase in arterial pressure during saralasin infusion. Arterial plasma concentration of norepinephrine did not differ between normal and sodiumdepleted dogs, nor did it change significantly after teprotide administration. These results suggest that, vessels, but has no significant effects on myocardial contractility or energetics. It also appears likely that the increase in cardiac output observed in sodiumdepleted dogs after angiotensin inhibition was caused, at least in part, by the decrease in systemic arterial pressure. INTRODUCTIONSodium depletion increases plasma renin activity (PRA)l and blood angiotensin II concentration (1-3), indicating an activation of the renin-angiotensin system. This increase in 'angiotensin II concentration probably plays an important role in the maintenance of normal arterial blood pressure during salt depletion, because the arterial blood pressure decreases under these conditions after administration of saralasin (1-sarcosine-8-alanine-angiotensin II; P113) (2-7), teprotide (SQ 20,881) (7-10), and SQ 14,225 (11). Saralasin is a competitive receptor antagonist of angiotensin II (4, 12, 13), whereas the latter two agents inhibit angiotensin-converting enzyme, which converts angiotensin I to the biologically active angiotensin II (8,(13)(14)(15)(16). Because angiotensin II is one of the most potent vasoconstrictors known (17, 18), a decrease in arterial blood pressure after angiotensin inhibition presumably is due to elimination of the angiotensin-induced vasoconstriction. However, angiotensin II also exerts a positive inotropic action on the heart (19,20), the abolition of which may lower the arterial pressure. Previous investigators (9, 10) have shown that cardiac output de-

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Section: Discussionmentioning

confidence: 50%

Section: Introductionmentioning

confidence: 99%

Renin-Angiotensin System Inhibition in Conscious Sodium-Depleted Dogs

Liang¹,

Gavras²,

Hood³

1978

J. Clin. Invest.

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“…In states of sodium depletion, there is increased secretion of renin by the renal juxtaglomerular cells leading to a rise in plasma angiotensin II (Vander, 1967;Boyd & Peart, 1971). It is well established for many species that angiotensin II has two important physiological actions (Peart, 1965). It is a potent arteriolar constrictor and it stimulates the zona glomerulosa of the adrenal to secrete aldosterone.…”

Section: Introductionmentioning

confidence: 99%

The effect of aldosterone and the renin‐angiotensin system on sodium, potassium and chloride transport by proximal and distal rat colon in vivo.

Dolman¹,

Edmonds²

1975

The Journal of Physiology

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SUMMARY1. The roles of aldosterone and angiotensin in the direct control of epithelial sodium transport in vivo have been investigated by measurement of electrical p.d. changes and of the fluxes of sodium, potassium and chloride in rat colon, an organ actively involved in electrolyte homoeostasis. Exogenous angiotensin and aldosterone were given by both short-and long-term infusions and endogenous secretion of the hormones was varied by dietary sodium variation and by nephrectomy and/or adrenalectomy.2. In vitro angiotensin has been shown to influence colonic salt and water absorption but in the present in vivo experiments administered angiotensin had no significant action on p.d. or on the ionic fluxes of the proximal or distal colon. The increase in p.d. produced by infusing aldosterone was unaffected by giving angiotensin concurrently. The effect of sodium depletion in stimulating sodium absorption and potassium secretion was completely abolished by adrenalectomy but was unaffected by nephrectomy.3. During prolonged infusion of angiotensin into adrenalectomized rats, a small fall in faecal fluid and sodium content was observed, but this change would have little significance in sodium homoeostasis.4. Aldosterone and sodium depletion stimulated sodium absorption in both proximal and distal colon but significant increase in potassium secretion was demonstrable only in the distal colon. Bicarbonate secretion (by calculation) was unaffected. In the proximal colon, the increased sodium absorption appeared to be accompanied by increased chloride absorption while in the distal colon it was principally the sodium-potassium exchange that was increased.

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“…Renin is a proteolytic enzyme that is secreted by the juxtaglomerular granular cells of the kidney and that catalyzes the release of angiotensin I from the renin substrate angiotensinogen (28,29). Angiotensin I is cleaved by angiotensinconverting enzyme (ACE) to form bioactive angiotensin II (28,29).…”

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confidence: 99%