Systemic and regional haemodynamic effects of a synthetic atrial natriuretic peptide in conscious rats

1986 ◽  
Vol 71 (3) ◽  
pp. 323-325 ◽  
Author(s):  
Carlos Caramelo ◽  
Arturo Fernandez-Cruz ◽  
Luis M. Villamediana ◽  
Elias Sanz ◽  
Diego Rodriguez-Puyol ◽  
...  

1. The effect of the intravenous injection of synthetic atrial natriuretic peptide (ANP, 2 μg) on systemic haemodynamics and blood flow to several organs has been studied in conscious rats by the radioactive microsphere technique. 2. ANP induced a 540% increase in sodium excretion and a 310% increase in urine flow. Mean arterial pressure decreased by 21 mmHg and the peripheral resistances decreased by 26%, without significant changes in cardiac output. 3. Renal blood flow increased by 37.7% and small intestine and portal blood flow increased by 39% and by 28% respectively. No other alterations in organ blood flows were observed. 4. From these data it can be concluded that atrial natriuretic peptide shows acute vascular relaxant properties, which seem to be specific for renal and mesenteric territories.

1986 ◽  
Vol 251 (1) ◽  
pp. G117-G123 ◽  
Author(s):  
L. Anzueto Hernandez ◽  
P. R. Kvietys ◽  
D. N. Granger

The postprandial intestinal hyperemia was studied in conscious and anesthetized rats using the radioactive microsphere technique. Carbohydrate, protein, lipid, and mixed meals, and the vehicle (Tyrode's solution), were placed in the stomach via a gastrostomy tube. In conscious rats, blood flow increased by 40-80% in the duodenum and jejunum 1 h after either a carbohydrate, lipid, protein, or mixed meal. Tyrode's solution produced a comparable hyperemia. Blood flow in the distal bowel segments (ileum, cecum, and colon) was significantly increased only by Tyrode'ds solution and the carbohydrate meal. The proximal intestinal hyperemia produced by the mixed meal in conscious animals was significantly attenuated by vagotomy yet unaltered by atropine pretreatment. In contrast to the results obtained from conscious rats, the mixed meal did not significantly alter intestinal blood flow in anesthetized animals. The results of this study indicate that the postprandial intestinal hyperemia is much greater in conscious than anesthetized animals. This difference may result from the higher resting blood flows in the latter group. The hyperemic response in conscious animals may be mediated by the vagus nerve.


1988 ◽  
Vol 74 (2) ◽  
pp. 207-211 ◽  
Author(s):  
A. Hughes ◽  
S. Thom ◽  
P. Goldberg ◽  
G. Martin ◽  
P. Sever

1. The effect of a α-human atrial natriuretic peptide (1–28) (ANP) on human vasculature was investigated in vivo and in vitro. Possible involvement of vascular dopamine receptors and the renin-angiotensin system in the response to ANP was also studied in vivo. 2. Forearm blood blow was measured by venous occlusion plethysmography. Isolated human blood vessels were studied using conventional organ bath techniques. 3. ANP (0.1–1 μg/min, intra-arterially) produced a dose-dependent increase in forearm blood flow, corresponding to a 163% increase in net forearm blood flow in the study arm. This action of ANP was not antagonized by (R)-sulpiride (100 μg/min, intra-arterially), a selective vascular dopamine receptor antagonist, or 50 mg of oral captopril, an inhibitor of angiotensin-converting enzyme. 4. ANP (1 nmol/l–1 μmol/l) produced concentration-dependent relaxation of isolated human arteries, including brachial artery, but was without effect on isolated human saphenous vein. 5. ANP produces vasodilatation in vivo and relaxes isolated human arterial smooth muscle. This action of ANP may contribute to its reported hypotensive effects in vivo.


1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.


1989 ◽  
Vol 256 (3) ◽  
pp. H760-H765 ◽  
Author(s):  
R. W. Lee ◽  
S. Goldman

To examine the mechanism by which atrial natriuretic peptide (ANP) decreases cardiac output, we studied changes in the heart, peripheral circulation, and blood flow distribution in eight dogs. ANP was given as a bolus (3.0 micrograms/kg) followed by an infusion of 0.3 microgram.kg-1.min-1. ANP did not change heart rate, total peripheral vascular resistance, and the first derivative of left ventricular pressure but decreased mean aortic pressure from 91 +/- 4 to 76 +/- 3 mmHg (P less than 0.001) and cardiac output from 153 +/- 15 to 130 +/- 9 ml.kg-1.min-1 (P less than 0.02). Right atrial pressure and left ventricular end-diastolic pressure also decreased. Mean circulatory filling pressure decreased from 7.1 +/- 0.3 to 6.0 +/- 0.3 mmHg (P less than 0.001), but venous compliance and unstressed vascular volume did not change. Resistance to venous return increased from 0.056 +/- 0.008 to 0.063 +/- 0.010 mmHg.ml-1.kg.min (P less than 0.05). Arterial compliance increased from 0.060 +/- 0.003 to 0.072 +/- 0.004 ml.mmHg-1.kg-1 (P less than 0.02). Total blood volume and central blood volume decreased from 82.2 +/- 3.1 to 76.2 +/- 4.6 and from 19.8 +/- 0.8 to 17.6 +/- 0.6 ml/kg (P less than 0.02), respectively. Blood flow increased to the kidneys. We conclude that ANP decreases cardiac output by decreasing total blood volume. This results in a lower operating pressure and volume in the venous capacitance system with no significant venodilating effects. Cardiac factors and a redistribution of flow to the splanchnic organs are not important mechanisms to explain the decrease in cardiac output with ANP.


1998 ◽  
Vol 21 (10) ◽  
pp. 737-742 ◽  
Author(s):  
Zenon S. Kyriakides ◽  
Eftihia Sbarouni ◽  
Aias Antoniadis ◽  
Efstathios K. Iliodromitis ◽  
Dimitrios Mitropoulos ◽  
...  

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