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)

Angiotensin I conversion and vascular reactivity in pathophysiological states in dogs

1980 ◽  
Vol 48 (2) ◽  
pp. 308-312 ◽  
Author(s):  
P. J. Leuenberger ◽  
S. A. Stalcup ◽  
L. M. Greenbaum ◽  
R. B. Mellins ◽  
G. M. Turino
Keyword(s):  
Blood Pressure ◽  
Enzyme Activity ◽  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Blood Pressure Response ◽  
Acute Hypoxia ◽  
Pressure Response ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Arterial Blood

To determine if angiotension converting enzyme activity is altered by acute pathophysiological insults, we assessed angiotensin I conversion using a blood pressure response technique in anesthetized dogs studied during acute 100% O2 breathing and acute acid-base derangements. Also, we determined systemic vascular reactivity to angiotensin II by measuring the magnitude and duration of the arterial blood pressure response to intra-arterial injections of angiotensin II under these same conditions. Angiotensin I conversion found in normoxia [91 +/- 7 (SD)%] was unchanged by acute acidosis, alkalosis, and hyperoxia. During acute hyperoxia the mean half time of the hypertensive response increased from 68 +/- 25 (SD) s at a PaO2 of 112 +/- 18 (SD) Torr to 100 +/- 34 (SD) s at a PaO2 of 491 +/- 47 (SD) Torr (P less than 0.01). No other pathophysiological condition studied had any effect on reactivity of systemic vasculature to angiotensin II. We conclude that, except during acute hypoxia as previously shown, converting enzyme activity is resistant to other pathophysiological insults and that vascular responsiveness to angiotensin II is enhanced by hyperoxia.

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.

Cardiovascular actions of microinjections of angiotensin II in the brain stem of rats

1984 ◽  
Vol 246 (5) ◽  
pp. R811-R816 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Brain Stem ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Ang Ii ◽  
The Brain

The blood pressure and heart rate responses to microinjection of angiotensin II (ANG II) into the brain stem of urethan-anesthetized rats were studied. Microinjection of ANG II into the area postrema (AP) resulted in significant elevation of blood pressure and significant reduction of heart rate. Microinjection into the region of the nucleus tractus solitarius (NTS) yielded a significant dose-dependent elevation in blood pressure and consistent increases in heart rate. The response to microinjection of ANG II into the region of the NTS was not due to leakage into the peripheral circulation, since intravenous administration of the ANG II antagonist, saralasin, did not attenuate the response. In fact, the cardiovascular response was increased after peripheral ANG II blockade, and the heart rate, which was consistently but not significantly elevated by NTS injection alone, was significantly elevated after saralasin pretreatment. Thermal ablation of the AP did not change the heart rate or the pressor response to microinjection of ANG II into the region of the NTS, indicating that the response was not mediated through the AP.

scholarly journals Arterial blood pressure response to heavy resistance exercise

1985 ◽  
Vol 58 (3) ◽  
pp. 785-790 ◽  
Author(s):  
J. D. MacDougall ◽  
D. Tuxen ◽  
D. G. Sale ◽  
J. R. Moroz ◽  
J. R. Sutton
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Valsalva Maneuver ◽  
Pressor Response ◽  
Intrathoracic Pressure ◽  
Pressure Response ◽  
Weight Lifting ◽  
Capacitance Transducer ◽  
Arterial Blood ◽  
Peak Pressures

The purpose of this study was to record the blood pressure response to heavy weight-lifting exercise in five experienced body builders. Blood pressure was directly recorded by means of a capacitance transducer connected to a catheter in the brachial artery. Intrathoracic pressure with the Valsalva maneuver was recorded as mouth pressure by having the subject maintain an open glottis while expiring against a column of Hg during the lifts. Exercises included single-arm curls, overhead presses, and both double- and single-leg presses performed to failure at 80, 90, 95, and 100% of maximum. Systolic and diastolic blood pressures rose rapidly to extremely high values during the concentric contraction phase for each lift and declined with the eccentric contraction. The greatest peak pressures occurred during the double-leg press where the mean value for the group was 320/250 mmHg, with pressures in one subject exceeding 480/350 mmHg. Peak pressures with the single-arm curl exercise reached a mean group value of 255/190 mmHg when repetitions were continued to failure. Mouth pressures of 30–50 Torr during a single maximum lift, or as subjects approached failure with a submaximal weight, indicate that a portion of the observed increase in blood pressure was caused by a Valsalva maneuver. It was concluded that when healthy young subjects perform weight-lifting exercises the mechanical compression of blood vessels combines with a potent pressor response and a Valsalva response to produce extreme elevations in blood pressure. Pressures are extreme even when exercise is performed with a relatively small muscle mass.

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.

Blunted blood pressure response to exercise and isolated muscle metaboreflex activation in patients with cirrhosis

2020 ◽  
Author(s):  
Pedro Augusto Carvalho Mira ◽  
Maria Fernanda Almeida Falci ◽  
Janaína Becari Moreira ◽  
Rosa Virginia Diaz Guerrero ◽  
Tarsila Campanha da Rocha Ribeiro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Pressure Response ◽  
Isometric Handgrip ◽  
Muscle Metaboreflex ◽  
Cirrhotic Patients ◽  
Response To Exercise

We sought to test the hypothesis that the cardiovascular responses to isolated muscle metaboreflex activation would be blunted in patients with cirrhosis. Eleven patients with cirrhosis and 15 healthy controls were evaluated. Blood pressure (BP, oscillometric method), contralateral forearm blood flow (FBF, venous occlusion plethysmography) and heart rate (HR, electrocardiogram) were measured during baseline, isometric handgrip at 30% of maximal voluntary contraction followed by post-exercise ischemia (PEI). Forearm vascular conductance (FVC) was calculated as follows: (FBF/mean BP) x 100. Changes in HR during handgrip were similar between groups, but tended to be different during PEI (controls: ∆0.5 ± 1.1 bpm vs. cirrhotic patients: ∆3.6 ± 1.0 bpm, P = 0.057). Mean BP response to handgrip (controls: ∆20.9 ± 2.7 mmHg vs. cirrhotic patients: ∆10.6 ± 1.5 mmHg, P = 0.006) and PEI was attenuated in cirrhotic patients (controls: ∆16.1 ± 1.9 mmHg vs. cirrhotic patients: ∆7.2 ± 1.4 mmHg, P = 0.001). In contrast, FBF and FVC increased during handgrip and decreased during PEI similarly between groups. These results indicate that an abnormal muscle metaboreflex activation explained, at least partially, the blunted pressor response to exercise exhibited by cirrhotic patients. Novelty bullets: • Patients with cirrhosis present abnormal muscle metaboreflex activation • Blood pressure response was blunted, but forearm vascular response was preserved • Heart rate response was slightly elevated

Role of the area postrema in angiotensin II modulation of baroreflex control of heart rate in conscious mice

2003 ◽  
Vol 284 (3) ◽  
pp. H1003-H1007 ◽  
Author(s):  
Baojian Xue ◽  
Hope Gole ◽  
Jaya Pamidimukkala ◽  
Meredith Hay
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Area Postrema ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Intravenous Infusions

This study reports the effects of angiotensin II (ANG II), arginine vasopression (AVP), phenylephrine (PE), and sodium nitroprusside (SNP) on baroreflex control of heart rate in the presence and absence of the area postrema (AP) in conscious mice. In intact, sham-lesioned mice, baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of ANG II were significantly less than those observed with similar increases in arterial pressure with PE (slope: −3.0 ± 0.9 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). Baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of AVP were the same as those observed with PE in sham animals (slope: −5.8 ± 0.7 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). After the AP was lesioned, the slope of baroreflex inhibition of heart rate was the same whether pressure was increased with ANG II, AVP, or PE. The slope of the baroreflex-induced increases in heart rate due to decreases in arterial blood pressure with SNP were the same in sham- and AP-lesioned animals. These results indicate that, similar to other species, in mice the ability of ANG II to acutely reset baroreflex control of heart rate is dependent on an intact AP.

Effects of nicotine and dietary salt on a learned blood pressure response in Dahl-S rats

2003 ◽  
Vol 284 (5) ◽  
pp. H1793-H1799 ◽  
Author(s):  
Justin H. Kuo ◽  
Richard O. Speakman ◽  
Aletia G. Sprinkle ◽  
Sheng-Gang Li ◽  
David R. Brown ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Pressure Response ◽  
High Salt ◽  
Dietary Salt ◽  
Arterial Blood ◽  
Behavioral Stress ◽  
Low Salt ◽  
External Stimuli

We examined the effects of chronic nicotine exposure and dietary salt on the arterial blood pressure (BP) changes learned in response to an acute behavioral stress in the Dahl salt-sensitive rat. Four groups were tested: low salt + vehicle; low salt + nicotine; high salt + vehicle; and high salt + nicotine. Rats were fed a low-salt (0.08% NaCl) or a high-salt (8% NaCl) diet for 4 wk; 2.4 mg · kg−1 · day−1nicotine or vehicle was given via an implanted osmotic minipump for the last 2 wk. All rats were conditioned by following one tone (CS+) with a 0.5-s tail shock; another tone (CS−) was never followed by shock. CS+ in low salt + vehicle and high salt + vehicle-treated rats evoked an initial arterial BP increase (C1), a component of the startle response, and an ensuing, smaller, but more sustained, pressor response (C2), which is acquired with training. In these rats, both C1 and C2 evoked by CS− were significantly smaller than those to CS+, demonstrating that these groups discriminated between the two tests. Conversely, although the low salt + nicotine-treated rats had both the C1 and C2 components of the conditional arterial pressure response, they did not discriminate between CS+ and CS−. Finally, the high salt + nicotine group failed to both discriminate between tones and acquire (i.e., learn) the C2 response. The unconditional response to shock did not differ between groups. We conclude that combined exposure to high salt and to nicotine inhibits the salt-sensitive animal's acquisition of a learned conditional BP response, perhaps because nicotine acts preferentially on those central processes required for associative learning versus those involved in orientating to external stimuli.

Sign in / Sign up

Export Citation Format

Share Document