Effects of tonin on the response to norepinephrine by the aortic strip of the hypertensive rat

1981 ◽  
Vol 59 (8) ◽  
pp. 790-793 ◽  
Author(s):  
R. Garcia ◽  
E. L. Schiffrin ◽  
G. Thibault ◽  
R. Boucher ◽  
J. Genest
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Aortic Smooth Muscle ◽  
Hypertensive Group ◽  
Aortic Strip ◽  
The One

The response to norepinephrine (NE) of arterial smooth muscle from two types of experimental hypertensive rats was investigated. Aortic strips from one-kidney, one-clip hypertensive animals were less responsive to NE than those from their normotensive controls but strips from two-kidney, one-clip hypertensive animals showed no difference from their corresponding controls. The contractility in response to NE was the same in all groups. These results suggest that the mechanisms responsible for the lesser reactivity in the one-kidney hypertensive group are not a consequence of elevated blood pressure itself but may be related to changes in the intrinsic sensitivity of aortic smooth muscle.Tonin potentiated the contraction induced by NE in aortic strips from hypertensive and normotensive rats. This effect was more pronounced in the one-kidney, one-clip hypertensive animals, so that although the aortic smooth muscle from these animals is less reactive to NE, the decreased reactivity can be more than compensated by the presence of tonin. The mechanism of potentiation is not yet clear but the fact that Saralasin did not inhibit it suggests that angiotensin Il is not generated in situ.

Effects of Tonin on Vascular Smooth Muscle of the Hypertensive Rat and Normal Rabbit

1980 ◽  
Vol 59 (s6) ◽  
pp. 339s-342s ◽  
Author(s):  
R. Garcia ◽  
E. L. Schiffrin ◽  
G. Thibault ◽  
R. Boucher ◽  
J. Genest
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Calcium Ion ◽  
Contractile Response ◽  
Control Group ◽  
Hypertensive Rats ◽  
Contralateral Kidney ◽  
Aortic Smooth Muscle ◽  
The One ◽  
Normotensive Control

1. The response of arterial smooth muscle to noradrenaline was studied in one-clip hypertensive rats with or without the contralateral/kidney and in normotensive rabbits. 2. Strips of aorta from one-kidney, one-clip hypertensive animals were less responsive to noradrenaline than normotensive control rats. The contractile response of strips from two-kidney, one-clip hypertensive animals was not different from the control group. These results suggest that the mechanisms responsible for the lesser reactivity in the one-kidney hypertensive group are not a consequence of elevated blood pressure itself, but may be related to the intrinsic contractility of aortic smooth muscle. 3. Tonin potentiated the contraction induced by noradrenaline in aortic strips from hypertensive and normotensive rats. However, this effect was more important in the one-kidney, one-clip hypertensive animals. In the aortic and mesenteric strips from normal rabbits, tonin produced not only potentiation to noradrenaline but direct contraction. 4. The potentiation to noradrenaline and the direct effect of tonin were not affected by a variety of antagonists but were blocked by a calcium ion antagonist, verapamil, suggesting that tonin may act directly on vascular smooth muscle through mechanisms which might be mediated by calcium ions.

Blood pressure recording in the ambulatory patient and evaluation of cardiovascular risk

1985 ◽  
Vol 68 (5) ◽  
pp. 485-488 ◽  
Author(s):  
Hans R. Brunner ◽  
Bernard Waeber ◽  
Jürg Nussberger
Keyword(s):  
Blood Pressure ◽  
Antihypertensive Therapy ◽  
Heart Attack ◽  
Blood Pressure Measurement ◽  
Epidemiological Studies ◽  
Cardiovascular Complications ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Intervention Trials ◽  
The One

Many large epidemiological studies, such as the one going on in Framingham [1], have clearly established that hypertension is one of the major risk factors for cardiovascular diseases. Well controlled intervention trials have also clearly demonstrated that antihypertensive therapy can significantly reduce the incidence of complications such as stroke, congestive heart failure and possibly myocardial infarction [2-4]. There exists no doubt about the important causal relationship between elevated blood pressure and cardiovascular complications. The measurement of blood pressure has thus become one of the most frequent procedures carried out by any practising physician. Notwithstanding, some doubt has been expressed whether all patients with a slightly elevated blood pressure at the physician's office are indeed prone to suffer a heart attack or a stroke and need lifelong antihypertensive therapy [5, 6]. Does the casual blood pressure measurement at the physician's office accurately assess the risk of each individual patient of suffering a heart attack in the future?

scholarly journals Therapeutic Relevance of Elevated Blood Pressure After Ischemic Stroke in the Hypertensive Rats

Hypertension ◽  
2020 ◽  
Vol 75 (3) ◽  
pp. 740-747
Author(s):  
Pratik C. Thakkar ◽  
Ailsa L. McGregor ◽  
P. Alan Barber ◽  
Julian F.R. Paton ◽  
Carolyn J. Barrett ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ischemic Stroke ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Therapeutic Relevance

Reduced contractile sensitivity and vasopressin receptor affinity in DOCA-salt hypertension

1992 ◽  
Vol 262 (6) ◽  
pp. H1752-H1758 ◽  
Author(s):  
C. S. Bockman ◽  
W. B. Jeffries ◽  
W. A. Pettinger ◽  
P. W. Abel
Keyword(s):  
Blood Pressure ◽  
Mesenteric Arteries ◽  
Elevated Blood Pressure ◽  
Vasopressin Receptor ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Receptor Affinity ◽  
Receptor Agonists ◽  
Salt Hypertension ◽  
Vasopressin Receptors

The affinity of vascular vasopressin receptors was studied to determine its role in altered vascular contractile sensitivity in deoxycorticosterone acetate (DOCA)-salt hypertension. Ring segments of rat mesenteric arteries were used to study vascular vasopressin receptors. Male Wistar rats were given subcutaneous injections of DOCA and 1% NaCl in the drinking water. Mesenteric arteries from hypertensive rats had a reduced contractile sensitivity to arginine vasopressin (AVP) and lysine vasopressin (LVP). The order of potency of vasopressin receptor agonists (AVP greater than LVP greater than oxytocin) was the same in arteries from hypertensive compared with normotensive animals. The affinity of the vasopressin receptor antagonist [deamino-Pen1,O-Me-Tyr2,Arg8] vasopressin, and the affinities of the vasopressin receptor agonists AVP and LVP were not altered during developing DOCA-salt hypertension. There was no change in contractile sensitivity to norepinephrine and KCl in arteries from hypertensive rats. The reduced vasopressin contractile sensitivity is not due to a change in vasopressin receptor affinity but may be a compensatory response to elevated blood pressure. These data suggest that increased vascular sensitivity does not contribute to elevated blood pressure during the developing stage of DOCA-salt hypertension.

Evidence against an increase in circulating pressor material in renal hypertensive rats

1960 ◽  
Vol 198 (6) ◽  
pp. 1148-1152 ◽  
Author(s):  
Pedro Blaquier ◽  
David F. Bohr ◽  
Sibley W. Hoobler
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Elevated Blood Pressure ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Test Animal ◽  
Renal Pedicle ◽  
Pressor Activity ◽  
Renal Hypertensive Rat ◽  
Renal Hypertensive Rats

The role played by circulating pressor substances in the renal hypertensive rat was studied by means of an isovolemic cross-circulation technique which is capable of detecting pressor activity in the blood of rats made hypertensive by continuous infusions of renin or synthetic angiotensin. When rats are made hypertensive by release of a completely occluded renal pedicle, this pressure elevation is transferred to an assay rat cross-circulated from the test animal several minutes after the release of the pedicle clamps. It follows that this form of renal hypertension is humorally mediated. On the contrary, when rats with renal hypertension of over 1 week's duration are cross-circulated no rise in blood pressure results in the assay rat, indicating that the maintenance of the elevated blood pressure in renal hypertension in the rat is not dependent on a circulating pressor material.

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