Dose-response study of the redistribution of intravascular volume by angiotensin II in man

1992 ◽  
Vol 82 (4) ◽  
pp. 397-405 ◽  
Author(s):  
Joseph G. Motwani ◽  
Allan D. Struthers
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Normal Male ◽  
Progressive Reduction ◽  
Venous Capacitance ◽  
Dose Response Study ◽  
Male Subjects

1. The response of systemic and regional haemodynamic indices to increasing infusion rates of angiotensin II (1, 3 or 10 ng min−1 kg−1) or placebo [5% (w/v) d-glucose] was studied in eight normal male subjects. 2. As compared with placebo, angiotensin II infusion caused an incremental rise in the serum angiotensin II level [14.5 ± 7.7 (placebo) to 187.2 ± 36.1 (10 ng of angiotensin II min−1 kg−1) pmol/l; mean ± 95% confidence interval] associated with a stepwise increase in total peripheral resistance [880 ± 42 (placebo) to 1284 ± 58 (10 ng of angiotensin II min−1 kg−1) dyn s cm−5] and a progressive reduction in cardiac output [8.3 ± 0.4 (placebo) to 7.0 ± 0.4 (10 ng of angiotensin II min−1 kg−1) litres/min]. 3. A stepwise fall in renal blood flow was observed with increasing angiotensin II infusion rate [1302 ± 65 (placebo) to 913 ± 64 (10 ng of angiotensin II min−1 kg−1) ml/min]. In contrast, calf blood flow was unaffected by 1 ng or 3 ng of angiotensin II min−1 kg−1 and was significantly increased by 10 ng of angiotensin II min−1 kg−1 (P < 0.01). 4. Calf venous capacitance was uninfluenced by 1 ng of angiotensin II min−1 kg−1, but was significantly increased by both 3 ng (P < 0.005) and 10 ng (P < 0.001) of angiotensin II min−1 kg−1. 5. Our results indicate that the pressor response to angiotensin II is a summation of multiple regional haemodynamic effects which differ qualitatively not only with the vascular bed studied but also within a single tissue, with the level of circulating angiotensin II attained. 6. The venodilatation we have demonstrated with high angiotensin II levels may effect a potentially favourable redistribution of blood flow in situations of inappropriate extracellular fluid volume expansion, such as chronic heart failure.

Angiotensin II: nitric oxide interaction and the distribution of blood flow

1993 ◽  
Vol 265 (6) ◽  
pp. R1276-R1283 ◽  
Author(s):  
D. H. Sigmon ◽  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Conscious Rats

Nitric oxide (NO) contributes to the regulation of regional blood flow. Inhibition of NO synthesis increases blood pressure and vascular resistance. Using radioactive microspheres and the substrate antagonist N omega-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg) to block NO synthesis, we tested the hypothesis that there is a significant interaction between the vasodilator NO and the vasoconstrictor angiotensin II, which regulates regional hemodynamics. Further, we investigated the influence of anesthesia on this interaction. L-NAME increased blood pressure, decreased cardiac output, and increased total peripheral resistance in both anesthetized and conscious rats. In anesthetized rats, L-NAME decreased blood flow to visceral organs (i.e. kidney, intestine, and lung) but had little effect on blood flow to the brain, heart, or hindlimb. Treating anesthetized rats with the angiotensin II receptor antagonist losartan (10 mg/kg) attenuated the decrease in cardiac output and the increase in total peripheral resistance without affecting the pressor response to L-NAME. Losartan also attenuated the visceral hemodynamic responses to L-NAME. In conscious rats, L-NAME decreased blood flow to all organ beds. Treating these rats with losartan only marginally attenuated the increase in total peripheral resistance to L-NAME without significantly affecting the pressor response or the decrease in cardiac output. Losartan had no effect on the regional hemodynamic responses to L-NAME. These data suggest that NO-mediated vascular relaxation is an important regulator of total peripheral and organ vascular resistance. (ABSTRACT TRUNCATED AT 250 WORDS)

Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Sexually Dimorphic ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Renal Vascular

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.

Angiotensin II induces insulin resistance independent of changes in interstitial insulin

1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucose Uptake ◽  
Peripheral Resistance ◽  
Glucose Turnover ◽  
Ang Ii

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.

scholarly journals Comparison of the Effects of Intravenous Papaverine Hydrochloride and Oral Pavabid HP Capsulets on Regional Cerebral Blood Flow in Normal Individuals

1983 ◽  
Vol 3 (4) ◽  
pp. 442-447 ◽  
Author(s):  
Lawrence C. McHenry ◽  
David A. Stump ◽  
George Howard ◽  
Thomas T. Novack ◽  
Don H. Bivins ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Normal Subjects ◽  
Normal Male ◽  
Regional Cerebral Blood ◽  
Normal Individuals ◽  
Left And Right ◽  
Male Subjects ◽  
Papaverine Hydrochloride

A single-blind study was conducted in 13 right-handed normal male subjects to compare the effects of oral and i.v. papaverine on regional cerebral blood flow (rCBF). Six xenon-133 inhalation rCBF measurements were performed on each subject; three tests—baseline, placebo, and drug evaluations—were carried out on each of two separate days. The oral and i.v. drugs were randomized for first-day administration. rCBF, measured as flow gray (FG), increased significantly (p ≤ 0.001) from baseline with both drug forms. Increases of 10.53% and 13.94% (left and right hemispheres, respectively) were demonstrated 90 min after a single 600-mg dose of oral papaverine. Increases of 5.09% and 8.69%, respectively, were recorded immediately after a single 100-mg dose of i. v. papaverine. FG also increased significantly (p ≤ 0.001) for both drug forms when compared to that of placebo. Placebo produced only a slight increase (not significant) with both the oral and i.v. groups. The data show that both oral and i.v. papaverine are equally effective in increasing rCBF in normal subjects.

ACTH Stimulates Plasma Renin and Angiotensin II in Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 273s-275s ◽  
Author(s):  
W. Oelkers ◽  
A. Köhler ◽  
L. Belkien ◽  
R. Fuchs-Hammoser ◽  
M. Maiga ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Normal Male ◽  
Renin Substrate ◽  
Trophic Effect ◽  
Physiological Regulator ◽  
Lag Period ◽  
Male Subjects

1. Adrenocorticotropic hormone (ACTH; 10 i.u./day) was infused for 34 h into normal male subjects. Some subjects were additionally treated with propranolol or indomethacin. Others received sham infusions or hydrocortisone infusions instead of ACTH. 2. ACTH, but not sham or hydrocortisone infusions, led to a significant increase in plasma renin activity and angiotensin II concentration with a lag period of 7–10 h and a maximum response after 24 h. ACTH may be a physiological regulator of renin secretion, perhaps through a ‘trophic’ effect on the juxtaglomerular apparatus. 3. The effect of ACTH on renin is not mediated by a rise in plasma renin substrate, probably not by renal β-adrenoreceptors, but perhaps by prostaglandins. 4. A dissociation between plasma cortisol and aldosterone during ACTH infusion suggests that ACTH, in this dosage, stimulates aldosterone on the second day through renin and angiotensin II, before its secretion is finally suppressed during more prolonged infusion.

The Clinical Measurement of Skeletal Blood Flow

1976 ◽  
Vol 50 (4) ◽  
pp. 261-268 ◽  
Author(s):  
R. Wootton ◽  
J. Reeve ◽  
N. Veall
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Transfer Rate ◽  
Random Noise ◽  
Extracellular Fluid ◽  
Normal Subjects ◽  
Normal Male ◽  
Physiological Variables ◽  
51Cr Edta ◽  
Absorbed Radiation Dose

1. A new method for measurement of skeletal blood flow is described which depends on the complete extraction of 18F in a single passage through bone. 2. Plasma concentration and urinary excretion are measured over a 2 h period. The technique of impulse analysis is used to determine the initial transfer rate of 18F to bone and extravascular extracellular fluid (ECF). The ECF component is evaluated by using a second tracer (51Cr-EDTA or 82Br) and the bone transfer rate obtained by difference. The 51Cr-EDTA data also provide an estimate of glomerular filtration rate and enable a correction to be applied for urinary bladder retention when necessary. 3. Duplicate measurements of skeletal blood flow in eight normal male volunteers gave mean flows between 4·4 and 5·9% of blood volume/min, or about 4 ml min−1 100 g−1 of bone. The variation between normal subjects was least when the results were expressed as % of blood volume/min rather than ml/min, ml min−1 kg−1 or ml min−1 1·73 m−2 body surface area. The precision of the technique was estimated to be 16·4%. 4. Addition of 1·5% random noise to the input data resulted in an uncertainty of 8·5% in the measurement of skeletal blood flow, suggesting that improved precision depends on closer control of physiological variables. 5. In six patients with severe untreated Paget's disease of bone, skeletal blood flow was 8·4–15·3% of blood volume/min. The increase was significant in all cases. 6. The absorbed radiation dose is low, so that the measurement can be repeated.

Aldosterone synthase gene variation and adrenocortical response to sodium status, angiotensin II and ACTH in normal male subjects

2004 ◽  
Vol 61 (2) ◽  
pp. 174-181 ◽  
Author(s):  
Brian Kennon ◽  
Mary C. Ingram ◽  
Elaine C. Friel ◽  
Niall H. Anderson ◽  
Scott M. MacKenzie ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Normal Male ◽  
Aldosterone Synthase ◽  
Gene Variation ◽  
Adrenocortical Response ◽  
Male Subjects
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