The contribution of the autonomic nervous system, the renin-angiotensin system and vasopressin to the maintenance of arterial blood pressure in adrenalectomized Wistar rats

1986 ◽  
Vol 71 (4) ◽  
pp. 357-365 ◽  
Author(s):  
S. M. Gardiner ◽  
T. Bennett
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Free Water ◽  
Renin Angiotensin System ◽  
Renin Angiotensin ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
Cardiovascular Actions ◽  
Ganglionic Transmission ◽  
Adrenalectomized Rats

1. Factors contributing to the maintenance of resting arterial blood pressure in sham-operated and adrenalectomized rats were assessed 14 weeks after operation; some animals were given 1% NaCl to drink throughout, and some animals were given sodium-free water instead of 1% NaCl for 2 days before the experiment. 2. Inhibition of the renin-angiotensin (ANG) system (with captopril) and of the cardiovascular actions of vasopressin [with 1-(β-mercapto-β,β-cyclopentamethylenepropionic acid), 8-d-arginine vasopressin (d(CH2)5DAVP)] had no hypotensive effects in sham-operated rats under any conditions, but antagonism of nicotinic ganglionic transmission (with pentolinium) caused a prompt fall in blood pressure. During combined administration of captopril, d(CH2)5DAVP and pentolinium to sham-operated rats, there was no significant recovery of blood pressure. 3. Adrenalectomized rats drinking 1% NaCl showed a marked hypotension and tachycardia in response to captopril, but d(CH2)5DAVP had little effect, whether administered before or after captopril. Addition of pentolinium rendered these animals more hypotensive man the sham-operated rats. 4. Adrenalectomized rats drinking sodium-free water for 2 days were hypotensive and blood pressures were lowered further by d(CH2)5DAVP or captopril under these conditions; there was no accompanying tachycardia. 5. The results indicate that, in chronically adrenalectomized rats drinking 1% NaCl, blood pressure is maintained by autonomic nervous and renin-ANG systems with no discernible contribution from the peripheral cardiovascular actions of vasopressin. However, the latter contribute importantly to the support of blood pressure when the adrenalectomized rats are rendered hypovolemic and hypotensive by substitution of sodium-free water to drink.

Terlipressin Versus  Norepinephrine to Correct Refractory Arterial Hypotension after General Anesthesia in Patients Chronically Treated with Renin-Angiotensin System Inhibitors

2003 ◽  
Vol 98 (6) ◽  
pp. 1338-1344 ◽  
Author(s):  
Gilles Boccara ◽  
Alexandre Ouattara ◽  
Gilles Godet ◽  
Eric Dufresne ◽  
Michèle Bertrand ◽  
...  
Keyword(s):  
Blood Pressure ◽  
General Anesthesia ◽  
Arterial Blood Pressure ◽  
Renin Angiotensin System ◽  
Arterial Hypotension ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Long Term Treatment ◽  
Systolic Arterial Blood Pressure

Background Terlipressin, a precursor that is metabolized to lysine-vasopressin, has been proposed as a drug for treatment of intraoperative arterial hypotension refractory to ephedrine in patients who have received long-term treatment with renin-angiotensin system inhibitors. The authors compared the effectiveness of terlipressin and norepinephrine to correct hypotension in these patients. Methods Among 42 patients scheduled for elective carotid endarterectomy, 20 had arterial hypotension following general anesthesia that was refractory to ephedrine. These patients were the basis of the study. After randomization, they received either 1 mg intravenous terlipressin (n = 10) or norepinephrine infusion (n = 10). Beat-by-beat recordings of systolic arterial blood pressure and heart rate were stored on a computer. The intraoperative maximum and minimum values of blood pressure and heart rate, and the time spent with systolic arterial blood pressure below 90 mmHg and above 160 mmHg, were used as indices of hemodynamic stability. Data are expressed as median (95% confidence interval). Results Terlipressin and norepinephrine corrected arterial hypotension in all cases. However, time spent with systolic arterial blood pressure below 90 mmHg was less in the terlipressin group (0 s [0-120 s] vs. 510 s [120-1011 s]; P < 0.001). Nonresponse to treatment (defined as three boluses of terlipressin or three changes in norepinephrine infusion) occurred in zero and eight cases (P < 0.05), respectively. Conclusions In patients who received long-term treatment with renin-angiotensin system inhibitors, intraoperative refractory arterial hypotension was corrected with both terlipressin and norepinephrine. However, terlipressin was more rapidly effective for maintaining normal systolic arterial blood pressure during general anesthesia.

scholarly journals Intermittent Hypoxia Increases Arterial Blood Pressure in Humans Through a Renin-Angiotensin System-Dependent Mechanism

Hypertension ◽  
2010 ◽  
Vol 56 (3) ◽  
pp. 369-377 ◽  
Author(s):  
Glen E. Foster ◽  
Patrick J. Hanly ◽  
Sofia B. Ahmed ◽  
Andrew E. Beaudin ◽  
Vincent Pialoux ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Intermittent Hypoxia ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Dependent Mechanism

The Effects of the Antagonists of the Renin—Angiotensin System on Cardiovascular Response to Lower-Body Subatmospheric Pressure in the Anaesthetized Cat

1980 ◽  
Vol 58 (6) ◽  
pp. 549-552 ◽  
Author(s):  
S. A. Adigun ◽  
D. P. Clough ◽  
J. Conway ◽  
R. Hatton
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Negative Pressure ◽  
Cardiovascular Response ◽  
Venous Pressure ◽  
Renin Angiotensin System ◽  
Lower Body ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

1. Lower-body subatmospheric (negative) pressure led to a prompt reduction in central venous pressure and arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. These reflex responses have been used to investigate the role angiotensin plays in blood pressure control. 2. The initial plasma renin activity (2.9 ng of angiotensin I h−1 ml−1) did not change during the brief lowering of pressure. Before pressure was lowered neither the angiotensin-converting enzyme inhibitor nor a competitive antagonist, [Sar1,Ala8]-angiotensin II, lowered arterial pressure. 3. Nevertheless, after inhibition of the renin-angiotensin system by these agents, the reduction in blood pressure induced by lower-body negative pressure became greater and the blood pressure recovery was impaired. 4. The findings suggest that angiotensin, at a blood concentration which has no direct effect on blood pressure, interacts with the sympathetic nervous system to maintain arterial blood pressure.

scholarly journals Vascular responsiveness in adrenalectomized rats with corticosterone replacement

1989 ◽  
Vol 256 (5) ◽  
pp. H1274-H1281 ◽  
Author(s):  
D. N. Darlington ◽  
K. Kaship ◽  
L. C. Keil ◽  
M. F. Dallman
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Arterial Blood Pressure ◽  
Body Weight Gain ◽  
Arterial Blood ◽  
Thymus Weight ◽  
Vascular Responsiveness ◽  
Vascular Sensitivity ◽  
Four Levels ◽  
Adrenalectomized Rats

To determine under resting, unstressed conditions the circulating glucocorticoid concentrations that best maintain sensitivity of the vascular smooth muscle and baroreceptor responses to vasoactive agents, rats with vascular cannulas were sham-adrenalectomized (sham) or adrenalectomized (ADRX) and provided with four levels of corticosterone replacement (approximately 100 mg fused pellets of corticosterone: cholesterol 0, 20, 40, and 80% implanted subcutaneously at the time of adrenal surgery). Changes in vascular and baroreflex responses were determined after intravenous injection of varying doses of phenylephrine and nitroglycerin with measurement of arterial blood pressure and heart rate in the conscious, chronically cannulated rats. Vascular sensitivity was decreased, and resting arterial blood pressure tended to be decreased in the adrenalectomized rats; both were restored to normal with levels of corticosterone (40%), which also maintained body weight gain, thymus weight, and plasma corticosteroid binding globulin concentrations at normal values. The baroreflex curve generated from the sham group was different from the curves generated from the ADRX+0, 20, and 40% groups, but not different from that of the ADRX+80% group, suggesting that the baroreflex is maintained by higher levels of corticosterone than are necessary for the maintenance of the other variables. These data demonstrate that physiological levels of corticosterone (40% pellet) restore vascular responsiveness, body weight, thymus weight, and transcortin levels to normal in ADRX rats, whereas higher levels (80% pellet) are necessary for restoration of the baroreflex.

Coevolution of the rennin–angiotensin system and the nervous control of blood circulation

1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.

Paraventricular stimulation with glutamate elicits bradycardia and pituitary responses

1989 ◽  
Vol 256 (1) ◽  
pp. R112-R119 ◽  
Author(s):  
D. N. Darlington ◽  
M. Miyamoto ◽  
L. C. Keil ◽  
M. F. Dallman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Arterial Blood Pressure ◽  
Excitatory Neurotransmitter ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
Paraventricular Nuclei ◽  
Measured Activation

The excitatory neurotransmitter, L-glutamate (0.5 M, pH 7.4), or the organic acid, acetate (0.5 M, pH 7.4), was microinjected (50 nl over 2 min) directly into the paraventricular nuclei (PVN) of pentobarbital sodium-anesthetized rats while arterial blood pressure and heart rate and plasma adrenocorticotropic hormone (ACTH), vasopressin, and oxytocin were measured. Activation of PVN neurons with L-glutamate led to increases in plasma ACTH, vasopressin, and oxytocin and a profound bradycardia (approximately 80 beats/min) with little change in arterial blood pressure. Microinjection of acetate had no effect on the above variables. The decrease in heart rate was shown to be dependent on the concentration of glutamate injected and the volume of injectate. The bradycardia was mediated through the autonomic nervous system because ganglionic blockade (pentolinium tartrate) eliminated the response; atropine and propranolol severely attenuated the bradycardia. The bradycardia was greatest when L-glutamate was microinjected into the caudal PVN. Injections into the rostral PVN or into nuclei surrounding the PVN led to small or nonsignificant decreases in heart rate. Focal electric stimulation (2-50 microA) of the PVN also led to decreases in heart rate and arterial blood pressure. These data suggest that activation of PVN neurons leads to the release of ACTH, vasopressin, and oxytocin from the pituitary and a bradycardia that is mediated by the autonomic nervous system.

Interactions between neural mechanisms, the renin-angiotensin system and vasopressin in the maintenance of blood pressure during water deprivation: studies in Long Evans and Brattleboro rats

1985 ◽  
Vol 68 (6) ◽  
pp. 647-657 ◽  
Author(s):  
S. M. Gardiner ◽  
T. Bennett
Keyword(s):  
Blood Pressure ◽  
Water Deprivation ◽  
Renin Angiotensin System ◽  
Neural Mechanisms ◽  
Brattleboro Rats ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Congenital Deficiency ◽  
Long Evans ◽  
Ganglionic Transmission

1. Plasma volumes and cardiovascular status were assessed in rats with a congenital deficiency in hypothalamic vasopressin (Brattleboro strain) and in the parent strain (Long Evans), in water-replete and water-deprived states. 2. Water-replete Brattleboro rats were not hypovolaemic; water deprivation (14 h in Brattleboro rats, 53 h in Long Evans rats) produced similar percentage reductions in plasma volumes in the two groups. 3. In the water-replete state, cardiovascular variables were similar in Long Evans and Brattleboro rats. Inhibition of ganglionic transmission (with pentolinium) or of the renin-angiotensin system (with captopril), separately, did not have a greater effect on blood pressure in Brattleboro rats than in Long Evans rats. Recovery from hypotension caused by pentolinium was characterized by large swings in blood pressure in both groups of rats. These pressor episodes were abolished by administration of captopril to Brattleboro rats. After administration of pentolinium and captopril to Long Evans rats there was a substantial, although intermittent, recovery in blood pressure that was abolished by an antagonist of the cardiovascular actions of vasopressin. 4. In the water-deprived state, blood pressures were similar in Long Evans and Brattleboro rats; both groups showed an elevation in diastolic blood pressure relative to the water-replete state. After administration of pentolinium, there was a more marked recovery in blood pressure than was seen in the water-replete state. Administration of Captopril alone had a slightly greater effect on blood pressure in Long Evans rats in the water-deprived, compared with the water-replete, state. However, in the former condition, Brattleboro rats showed a profound and progressive hypotension in response to captopril, indicating an indispensable role for the renin-angiotensin system in the maintenance of blood pressure in these animals during water deprivation. 5. Only when the renin-angiotensin system and neural activity were inhibited did vasopressin express its full, independent, pressor potential in Long Evans rats. However, evidence was obtained that vasopressin may exert important effects on cardiovascular regulation via neural mechanisms and through interactions with the renin-angiotensin system.

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