Comparative study of pressor and heart rate responses to angiotensin II and noradrenaline in pregnant and non-pregnant women

1992 ◽  
Vol 82 (2) ◽  
pp. 157-162 ◽  
Author(s):  
Margaret Ramsay ◽  
Fiona Broughton Pipkin ◽  
Peter Rubin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Pregnant Women ◽  
Arterial Blood Pressure ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Arterial Blood ◽  
Diastolic Arterial Blood Pressure ◽  
In Pregnancy

1. Twenty-eight healthy non-pregnant women and 28 women in the first or second trimester of pregnancy were studied. They were given an incremental intravenous infusion of either noradrenaline or angiotensin II. Pressor and heart rate responses were documented. 2. Dose-pressor response curves were constructed for the two agents in pregnant and non-pregnant women (n=14 in each group). The regression parameters of slope and intercept were calculated, and were used to derive the variables of dose required to elicit a 10 mmHg rise in systolic or diastolic blood pressure. 3. The pressor response to angiotensin II was diminished in pregnancy, with approximately twice the dose being required to raise the systolic or diastolic arterial blood pressure as in non-pregnant subjects. 4. The systolic pressor response to noradrenaline was slightly diminished in pregnancy, but the diastolic pressor response was unchanged. There were no significant differences between the doses of noradrenaline required to elicit a 10 mmHg rise in systolic or diastolic arterial blood pressure in pregnant or non-pregnant subjects. 5. There was a diminution in the bradycardia evoked in response to both hormones in pregnancy. 6. We conclude that the well-documented pressor insensitivity to angiotensin II during pregnancy is a specific phenomenon, not a manifestation of a generalized reduction in vascular reactivity.

Effects of the angiotensin II receptor antagonist Losartan (DuP 753/MK 954) on arterial blood pressure, heart rate, plasma concentrations of angiotensin II and renin and the pressor response to infused angiotensin II in the salt-deplete dog

1992 ◽  
Vol 83 (5) ◽  
pp. 549-556 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Plasma Angiotensin

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1–3 μmin−1 kg−1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min−1kg−1), and a dose of 10 μgmin−1 kg−1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 μmin−1 kg−1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 ± 11.2 to 95.0 ± 12.8 mmHg) and a rise in heart rate (from 84.6 ± 15.1 to 103 ± 15.2 beats/min). Baseline plasma angiotensin II (42.5 ± 11.8 pg/ml) and renin (64.5 ± 92.7 μ-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 ± 11.6 mmHg) was reduced at 15 min (11.8 ± 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 ± 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ngmin−1kg−1, +19.9 ± 8 mmHg; 2000ngmin−1 kg−1, +52.8 ± 13.9 mmHg) with a fall in heart rate (1000 ng min−1 kg−1, −27.9 ± 11.5 beats/min; 2000 ng min−1 kg−1, −31.2 ± 17.3 beats/min). During Losartan infusion the 1000 but not the 2000 ng min−1 kg−1 noradrenaline infusion caused a greater rise in mean arterial blood pressure and a greater fall in heart rate. The fall in heart rate tended to decrease with continued infusion of Losartan. Plasma catecholamine concentrations were unaffected by Losartan. In a further study, higher doses of Losartan (100, 300 and 1000 μg min−1 kg−1; 30 min) produced greater falls in mean arterial blood pressure also with a rise in heart rate and complete blockade of the pressor effect of infused angiotensin II. Some animals became disturbed at the highest dose. 3. Losartan produces rapid dose-related falls in blood pressure and a rise in heart rate and renin release with elevation of plasma angiotensin II. Pressor responses to angiotensin II are reduced at intermediate doses and are eliminated at high doses. Losartan does not appear to inhibit angiotensin II clearance from the plasma and may in some way increase it.

Cardiovascular consequences of microinjection of vasopressin and angiotensin II in the area postrema

1993 ◽  
Vol 265 (3) ◽  
pp. R625-R631 ◽  
Author(s):  
V. L. Lowes ◽  
L. E. McLean ◽  
N. W. Kasting ◽  
A. V. Ferguson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Area Postrema ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Systemic Administration ◽  
Pressure Response ◽  
Arterial Blood ◽  
At1 Antagonist

Microinjection of angiotensin II (ANG II) into the area postrema (AP) of urethan-anesthetized male Sprague-Dawley rats elicited statistically significant increases in mean arterial blood pressure at doses ranging from 10 pg to 500 ng (10 pg, mean +/- SE, 10.8 +/- 1.1 mmHg, P < 0.001; 250 ng, 15.2 +/- 2.6 mmHg, P < 0.001). Heart rate was also significantly increased at doses > 10 pg, although these increases were not dose dependent. Systemic administration of losartan (Dup-753), an AT1 antagonist, was able to significantly reduce the pressor response to 250 ng ANG (post-losartan: 81.9 +/- 9.5% reduction in blood pressure response, P < 0.0001), whereas PD123319, an AT2 antagonist, was without significant effect (P > 0.1). Microinjection of vasopressin (VP) (10 pg-500 ng) into the AP also resulted in statistically significant increases in blood pressure at doses ranging from 10 to 100 pg (10 pg, 7.0 +/- 1.5 mmHg, P < 0.05) and 100-500 ng (250 ng, 12.2 +/- 1.8 mmHg, P < 0.0001). Small but significant changes in heart rate were observed only at 100 pg and 100 ng. Systemic administration of a V1 antagonist significantly attenuated the increases in blood pressure in response to 50, 100, and 250 ng VP (250 ng, post-V1 antagonist: 66.4 +/- 8.6% reduction in blood pressure response, P < 0.001), whereas [desamino,D-Arg8]vasopressin (DDAVP), a V2 agonist, had a depressor effect when microinjected directly into the AP (250 ng, -9.9 +/- 1.6 mmHg, P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of adenosine-1 receptor-mediated preglomerular vasoconstriction in AT1Areceptor-deficient mice

1998 ◽  
Vol 275 (6) ◽  
pp. F922-F927 ◽  
Author(s):  
Timothy Traynor ◽  
Tianxin Yang ◽  
Yuning G. Huang ◽  
Lois Arend ◽  
Michael I. Oliverio ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Knockout Mice ◽  
Vascular Reactivity ◽  
Feedback System ◽  
Tubuloglomerular Feedback ◽  
Arterial Blood ◽  
Simultaneous Activation ◽  
Arteriolar Tone

The effect of the adenosine type 1 receptor agonist N 6-cyclohexyladenosine (CHA) on glomerular vascular reactivity was studied in male angiotensin II type 1A (AT1A) receptor knockout mice (9). Vascular reactivity was assessed as the response of stop-flow pressure (PSF) to infusion of CHA into loops of Henle using micropuncture techniques. In AT1A +/+ mice at ambient arterial blood pressure (96.7 ± 2.8 mmHg), the presence of CHA (10−5 M) in the perfusate increased PSF responses from 6.8 ± 0.6 to 14.3 ± 0.9 mmHg when the loop of Henle of the index nephron was perfused and from 0.7 ± 0.3 to 12.3 ± 1.0 mmHg when the loop of an adjacent nephron was perfused. At reduced arterial blood pressure (82.8 ± 1.3 mmHg), index nephron perfusion with CHA increased PSF responses from 4.5 ± 0.3 to 9.4 ± 0.4 mmHg. In AT1A −/− mice with a mean arterial blood pressure of 80 ± 1.9 mmHg, CHA increased PSF responses only from 0.1 ± 0.3 to 3.6 ± 0.54 mmHg during index nephron perfusion and from 0.25 ± 0.2 to 2.7 ± 0.55 mmHg during adjacent nephron perfusion, significantly less than in wild-type animals ( P < 0.001). Responses to CHA were intermediate in AT1A +/− mice. Thus AT1A receptor knockout mice show a markedly reduced constrictor response to CHA both in the presence and absence of simultaneous activation of the tubuloglomerular feedback system. These data support the notion of a functional interaction between adenosine and angiotensin II in the regulation of afferent arteriolar tone.

Plasma vasopressin in blood pressure homeostasis and in experimental renal hypertension

1980 ◽  
Vol 239 (1) ◽  
pp. H81-H87 ◽  
Author(s):  
P. T. Pullan ◽  
C. I. Johnston ◽  
W. P. Anderson ◽  
P. I. Korner
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Renal Hypertension ◽  
Similar Degree ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Experimental Renal Hypertension

The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension was investigated in the conscious dog. Intravenous infusion of synthetic arginine vasopressin to elevate plasma levels approximately fivefold to 31 pg/ml caused bradycardia in normal dogs, together with suppression of plasma renin activity and angiotensin II. This plasma level of vasopressin also caused elevation of mean arterial blood pressure in dogs with pharmacological total autonomic blockade. A similar degree of elevation of plasma vasopressin concentration was observed following mild nonhypotensive hemorrhage; more severe hemorrhage resulted in an approximate 100-fold increase in plasma vasopressin levels. Severe renal artery constriction in unilaterally nephrectomized dogs caused a marked rise in mean arterial blood pressure, but only a doubling of plasma vasopressin concentration. A suppressor infusion of vasopressin did not potentiate the pressor response to infused angiotensin II. It is concluded that vasopressin may play a role in normal cardiovascular homeostatic responses, but it is unlikely to have a significant direct vasoconstrictor role in the pathogenesis of this form of experimental renal hypertension.

Sex differences in central cholinergic and angiotensinergic control of vasopressin release

1992 ◽  
Vol 263 (5) ◽  
pp. R1030-R1034 ◽  
Author(s):  
J. D. Stone ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Estrous Cycle ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Female Rats ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin

In conscious, unrestrained rats, the intracerebroventricular injection of the cholinergic agonist, carbachol, or angiotensin II resulted in the transient stimulation of vasopressin secretion, elevation of mean arterial blood pressure, and reduction of heart rate. After the injection of carbachol (25 ng) into a lateral cerebral ventricle, the plasma vasopressin concentration in male rats was increased to twice that of female rats in each phase of the estrous cycle; mean arterial blood pressure was elevated more in males than females, whereas heart rate fell to the same extent in both sexes. In contrast, the increase in the plasma vasopressin concentration of males after the injection of angiotensin II (20 ng) was one-half that of females, and the hypertensive and bradycardic responses were similar in both sexes. Phase of the female estrous cycle had no effect on the responses to either agent. These findings indicate that central cholinergic and angiotensinergic mechanisms controlling vasopressin release are influenced differently by gender. The role of the gonadal steroid hormones in these mechanisms remains to be determined.

Compression Stocking Length Effects on Arterial Blood Pressure and Heart Rate Following Head-Up Tilt in Healthy Volunteers

2014 ◽  
Vol 63 (6) ◽  
pp. 435-438 ◽  
Author(s):  
Kunihiko Tanaka ◽  
Shiori Tokumiya ◽  
Yumiko Ishihara ◽  
Yumiko Kohira ◽  
Tetsuro Katafuchi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Healthy Volunteers ◽  
Arterial Blood Pressure ◽  
Compression Stocking ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
Length Effects
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