Effect of Angiotensin II on the Intact Forearm Veins of Man

Pasquale, N. P. De; Burch, George E.

doi:10.1161/01.res.13.3.239

Cited by 43 publications

(13 citation statements)

References 7 publications

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“…It is conceivable that release of renin from the kidney by furosemide with subsequent angiotensin II production could have caused generation of a vasodilator substance in the vasculature to produce the effects we observed. In contrast to its profound effects on arterioles, angiotensin II produces little or no direct constriction of capacitance vessels (DePasquale and Burch, 1963;Somlyo and Sorrilyo, 1966). It has been observed in several vascular beds that angiotensin II stimulates production of a vasodilator prostaglandin that modulates the arteriolar constriction produced by angiotensin (Messina et al, 1976;Gryglewski et al, 1980).…”

Section: Discussionmentioning

confidence: 99%

Factors modifying the early nondiuretic vascular effects of furosemide in man. The possible role of renal prostaglandins.

Johnston¹,

Hiatt²,

Nies³

et al. 1983

Circulation Research

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Animal experiments have suggested that salt-balance, prostaglandin synthesis, and renal function are important determinants of the nondiuretic vascular effects of furosemide. To investigate the influence of these factors in humans, we studied 10 normal volunteers and five anephric patients. The volunteers were studied on three occasions: when on a 10 mEq/day sodium diet, on a 250 mEq/day sodium diet, and on a 10 mEq/day sodium diet with indomethacin, 200 mg/day. The anephric patients were studied immediately after dialysis. Plethysmographic methods were used to measure venous capacitance and blood flow in the calf before, and at 5, 10, and 15 minutes after furosemide, 80 mg, iv. Blood was obtained before and 15 minutes after furosemide for determination of plasma renin activity by radioimmunoassay and of plasma 6-keto-prostaglandin F1 alpha by chromatography-mass spectrometry. We found that furosemide significantly increased venous capacitance in the calf of the normal volunteers on a low salt diet. Indomethacin, high salt intake, or lack of renal function was sufficient to inhibit this effect. Plasma renin activity increased only in the group that had the increase in venous capacitance. Limb blood flow decreased gradually in the 15 minutes following administration of furosemide in the normal volunteers, regardless of salt balance or indomethacin, but remained unchanged in the anephric patients. Plasma 6-keto-prostaglandin F1 alpha was less than 30 pg/ml in all samples. Indomethacin concentration averaged 1.3 micrograms/ml in volunteers on the drug. To determine whether indomethacin, salt intake or renal function affected another venodilator, we studied an additional group of normal and uremic volunteers who received 0.6 mg nitroglycerin sublingually.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Factors modifying the early nondiuretic vascular effects of furosemide in man. The possible role of renal prostaglandins.

Johnston¹,

Hiatt²,

Nies³

et al. 1983

Circulation Research

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“…The temperature change suggests the mechanism is venous constriction as described for levarterenol. However, injection of angiotensin into an intact isolated segment of a large superficial vein in the human forearm produces little evidence of venous constriction (56), and local administration has little effect on the veins of animals (2,8,55,57). On the other hand, intravenous administration produces a slight rise in the pressure within the intact presumably isolated segment of superficial forearm vein (56) and a decrease in forearm venous compliance (58).…”

Section: Discussionmentioning

confidence: 99%

Responses of the Human Upper Extremity Vascular Bed to Exercise, Cold, Levarterenol, Angiotensin, Hypertension, Heart Failure, and Respiratory Tract Infection with Fever *

Kettel¹,

Overbeck²,

Daugherty³

et al. 1964

J. Clin. Invest.

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“…Thus; the volume and/ or renin state prior to the administration of the inhibitor may determine the venous response and may explain the contrasting claims by previous investigators as some have reported that angiotensin II has a marked venoconstrictive effect (DePasqualle and Burch, 1963) but this was not confirmed by others (Tsuru et al, 1976). These discrepant results may also reflect differences due to varying bradykinin levels, since it is known that the converting enzyme inhibitor may potentiate the action of bradykinin (see below), which relaxes venous smooth muscle (Levy, 1972).…”

Section: Hemodynamic Effects Of Converting Enzyme Inhibitor In Normalmentioning

confidence: 98%

Role of the renin-angiotensin system in blood pressure regulation. The cardiovascular effects of converting enzyme inhibition in normotensive subjects.

Niarchos¹,

Pickering²,

Case³

et al. 1979

Circulation Research

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SUMMARYThe role of the renin-angiotensin system in the regulation of blood pressure in normal human subjects was investigated by administering to them the converting enzyme inhibitor (SQ 20881) during sodium-replete and sodium-depleted states. In the sodium-replete state (150 m£q sodium intake for 5 days) in eight normal subjects, converting enzyme inhibitor decreased the average mean arterial pressure from 75 ± 4 to 65 ± 5 mm Hg (P < 0.005) because of a decrease in peripheral resistance from 17 ± 1 to 14 ± 1 U (P < 0.025). Cardiac output did not change because of a simultaneous decrease in venous return. Sodium depletion (10 mEq sodium intake for 5 days) in six subjects resulted in an insignificant decrease in blood pressure (from 7 5 ± 4 t o 6 9 ± 2 mm Hg), whereas cardiac output decreased from 5.15 ± 0.29 to 3.91 ± 0.22 liters/min (P < 0.05). Plasma renin activity increased with sodium depletion from 2.13 ± 0.38 to 7.3 ± 1.3 ng/ml per hour (P< 0.005). Converting enzyme inhibitor administration in the sodium-depleted state (n » 8) decreased mean arterial pressure from 69 ± 2 to 53 ± 5 mm Hg (P < 0.005) because of a decrease in peripheral resistance from 18 ± 1 to 12 ± 1 U (P < 0.005), whereas cardiac output increased from 3.91 ± 0.33 to 4.40 ± 0.30 liters/min (P < 0.005). The maximum decrease in diastolic blood pressure caused by the inhibitor correlated to the control plasma renin activity (r = 0.76, P < 0.01, n =• 14 measurements). These results indicate that the renin-angiotensin system participates in the regulation of blood pressure and cardiac function in normal subjects, even in the sodium-replete state. This role of the renin-angiotensin system in cardiovascular homeostasis in normal subjects becomes more crucial during sodium depletion when plasma renin (angiotensin II) is markedly increased. Cux Res 45:839-837, 1979 RECENT studies (Laragh, 1978) have provided evidence supporting a possible role for the reninangiotensin system in the pathogenesis and maintenance of elevated arterial pressure in essential and renovascular hypertension in human subjects. This pathogenetic role of angiotensin II has been investigated more precisely because of the availability, initially, of the angiotensin II competitive antagonist, saralasin (P 113), and, more recently, of the inhibitors of the angiotensin-converting enzyme. These agents, unlike saralasin, have no intrinsic agonistic activity, since they act by blocking the conversion of angiotensin I to angiotensin II, thereby eliminating the cardiovascular and endocrine effects of circulating angiotensin II. However, the participation of the renin-angiotensin system in the regulation of arterial pressure in normal human subjects has not been characterized fully because so far no complete hemodynamic measurements have been performed in normal subjects during converting enzyme inhibition. Haber and associates (Sancho et al., 1976;Haber, 1976), by administering the converting enzyme inhibitor in sodium-repleted and sodium-deprived normal subjects, concluded that angio...

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Effect of Angiotensin II on the Intact Forearm Veins of Man

Cited by 43 publications

References 7 publications

Factors modifying the early nondiuretic vascular effects of furosemide in man. The possible role of renal prostaglandins.

Factors modifying the early nondiuretic vascular effects of furosemide in man. The possible role of renal prostaglandins.

Responses of the Human Upper Extremity Vascular Bed to Exercise, Cold, Levarterenol, Angiotensin, Hypertension, Heart Failure, and Respiratory Tract Infection with Fever *

Role of the renin-angiotensin system in blood pressure regulation. The cardiovascular effects of converting enzyme inhibition in normotensive subjects.

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