A Circulating Humoral Pressor Agent in Dahl S Rats with Salt Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 345s-347s ◽  
Author(s):  
L. Tobian ◽  
Mary Pumper ◽  
Susan Johnson ◽  
J. Iwai
Keyword(s):  
Vascular Resistance ◽  
Vasoconstrictor Effect ◽  
Salt Hypertension ◽  
Humoral Agent ◽  
Pressor Agent

1. In Dahl S rats becoming hypertensive while on a diet of high NaCl content there appears to be a blood-borne humoral agent which produces vasoconstriction in a bioassay using the isolated hindquarters of rats. 2. This vasoconstrictor effect strongly suggests the presence of a humoral pressor agent or the lack of a vasodilator agent in the blood of hypertensive S rats. 3. The vasoconstrictor effect is not due to high renin concentrations. 4. This humoral vasoconstrictor action could partly account for the high vascular resistance in the hypertensive S rat.

scholarly journals Vasodilator tone in the llama fetus: the role of nitric oxide during normoxemia and hypoxemia

2005 ◽  
Vol 289 (3) ◽  
pp. R776-R783 ◽  
Author(s):  
Emilia M. Sanhueza ◽  
Raquel A. Riquelme ◽  
Emilio A. Herrera ◽  
Dino A. Giussani ◽  
Carlos E. Blanco ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Control Group ◽  
Blood Flows ◽  
Vasoconstrictor Effect ◽  
Vascular Beds ◽  
Oxide Synthase

The fetal llama responds to hypoxemia, with a marked peripheral vasoconstriction but, unlike the sheep, with little or no increase in cerebral blood flow. We tested the hypothesis that the role of nitric oxide (NO) may be increased during hypoxemia in this species, to counterbalance a strong vasoconstrictor effect. Ten fetal llamas were operated under general anesthesia. Mean arterial pressure (MAP), heart rate, cardiac output, total vascular resistance, blood flows, and vascular resistances in cerebral, carotid and femoral vascular beds were determined. Two groups were studied, one with nitric oxide synthase (NOS) blocker NG-nitro-l-arginine methyl ester (l-NAME), and the other with 0.9% NaCl (control group), during normoxemia, hypoxemia, and recovery. During normoxemia, l-NAME produced an increase in fetal MAP and a rapid bradycardia. Cerebral, carotid, and femoral vascular resistance increased and blood flow decreased to carotid and femoral beds, while cerebral blood flow did not change significantly. However, during hypoxemia cerebral and carotid vascular resistance fell by 44% from its value in normoxemia after l-NAME, although femoral vascular resistance progressively increased and remained high during recovery. We conclude that in the llama fetus: 1) NO has an important role in maintaining a vasodilator tone during both normoxemia and hypoxemia in cerebral and femoral vascular beds and 2) during hypoxemia, NOS blockade unmasked the action of other vasodilator agents that contribute, with nitric oxide, to preserving blood flow and oxygen delivery to the tissues.

Circulatory responses to hypocapnia in the anesthetized dog

1965 ◽  
Vol 208 (1) ◽  
pp. 139-143 ◽  
Author(s):  
Hermes A. Kontos ◽  
H. Page Mauck ◽  
David W. Richardson ◽  
John L. Patterson
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Positive Pressure ◽  
Arterial Blood ◽  
Vasoconstrictor Effect ◽  
Anesthetized Dogs ◽  
Intact Limb

The circulatory responses to hypocapnia were studied in 40 anesthetized dogs. Hypocapnia induced without a change in ventilation caused slight increase in limb vascular resistance in six dogs and decrease in one. Hypocapnia induced by hyperventilation caused increase in limb vascular resistance in six dogs and decrease in four. Following administration of phenoxybenzamine into the femoral artery, hypocapnia induced by either method invariably caused increase in limb vascular resistance (8 dogs). These results show that hypocapnia has a direct vasoconstrictor effect on limb blood vessels. In the intact limb this response may be opposed by vasodilator effects mediated through nerves. Hypocapnia induced without change in ventilation had no significant effect on cardiac output, systemic vascular resistance or arterial blood pressure (8 dogs). Hypocapnia induced by increased ventilation was associated with significant decreases in cardiac output and systemic arterial blood pressure and significant increase in systemic vascular resistance (9 dogs). These responses were probably related to the effects of increased intermittent positive pressure used to augment ventilation.

Intrarenal Formation of Angiotensin II in the Rat: Interference by Saralasin and SQ 20881

1974 ◽  
Vol 48 (s2) ◽  
pp. 37s-40s
Author(s):  
H. Zschiedrich ◽  
K. G. Hofbauer ◽  
E. Hackenthal ◽  
G. D. Baron ◽  
F. Gross
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Renal Vascular Resistance ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Vasoconstrictor Effect ◽  
Renal Vascular ◽  
Dose Dependent

1. Isolated rat kidneys were perfused with a medium free of components of the renin-angiotensin system. 2. Angiotensin II, angiotensin I, tetradecapeptide renin substrate or rat plasma renin substrate added to the medium caused a dose-dependent increase of renal vascular resistance. 3. The vasoconstrictor effect of angiotensin II was inhibited by 1-Sar-8-Ala-angiotensin II (Saralasin). The inhibition was dose-dependent, being complete at the highest doses applied. In this dose range, Saralasin increased renal vascular resistance. Saralasin also inhibited vasoconstriction induced by tetradecapeptide renin substrate. 4. The vasoconstrictor effect of angiotensin I was suppressed by SQ 20881, up to a maximum of 87% depending on the dose. Similarly the increase in renal vascular resistance induced by a purified preparation of rat plasma renin substrate was inhibited by 55%; no effect on the action of tetradecapeptide renin substrate was observed. 5. The data suggest that, within the kidney, angiotensin I is converted into angiotensin II to the extent of about 1.25%. Since no angiotensin I is formed from synthetic renin substrate, the vasoconstrictor effect of the tetradecapeptide may be either due to a direct interaction with the angiotensin II receptor or the consequence of the intrarenal formation of angiotensin II. In contrast, the results with rat plasma renin substrate suggest that angiotensin I is formed from ‘natural’ substrate and is subsequently converted into angiotensin II.

scholarly journals Time-dependent changes in autonomic control of splanchnic vascular resistance and heart rate in ANG II-salt hypertension

2012 ◽  
Vol 302 (3) ◽  
pp. H763-H769 ◽  
Author(s):  
Marcos T. Kuroki ◽  
Pilar A. Guzman ◽  
Gregory D. Fink ◽  
John W. Osborn
Keyword(s):  
Heart Rate ◽  
Vascular Resistance ◽  
Sympathetic Nerve Activity ◽  
Autonomic Control ◽  
Ang Ii ◽  
Resistance Arteries ◽  
Low Salt ◽  
Salt Hypertension ◽  
Mesenteric Artery Blood Flow ◽  
Mesenteric Vascular Resistance

Previous studies suggest that ANG II-induced hypertension in rats fed a high-salt (HS) diet (ANG II-salt hypertension) has a neurogenic component dependent on an enhanced sympathetic tone to the splanchnic veins and independent from changes in sympathetic nerve activity to the kidney or hind limb. The purpose of this study was to extend these findings and test whether altered autonomic control of splanchnic resistance arteries and the heart also contributes to the neurogenic component. Mean arterial pressure (MAP), heart rate (HR), superior mesenteric artery blood flow, and mesenteric vascular resistance (MVR) were measured during 4 control days, 14 days of ANG II delivered subcutaneously (150 ng·kg−1·min−1), and 4 days of recovery in conscious rats fed a HS (2% NaCl) or low-salt (LS; 0.1% NaCl) diet. Autonomic effects on MAP, HR, and MVR were assessed by acute ganglionic blockade with hexamethonium (20 mg/kg iv) on day 3 of control, days 1, 3, 5, 7, 10, and 13 of ANG II, and day 4 of recovery. MVR increased during ANG II infusion in HS and LS rats but remained elevated only in HS rats. Additionally, the MVR response to hexamethonium was enhanced on days 10 and 13 of ANG II selectively in HS rats. Compared with LS rats, HR in HS rats was higher during the 2nd wk of ANG II, and its response to hexamethonium was greater on days 7, 10, and 13 of ANG II. These results suggest that ANG II-salt hypertension is associated with delayed changes in autonomic control of splanchnic resistance arteries and the heart.

scholarly journals The Neurogenic Vasoconstrictor Effect of Digitalis on Coronary Vascular Resistance

1974 ◽  
Vol 53 (1) ◽  
pp. 288-296 ◽  
Author(s):  
Nason P. Hamlin ◽  
James T. Willerson ◽  
Hasan Garan ◽  
William John Powell
Keyword(s):  
Vascular Resistance ◽  
Coronary Vascular Resistance ◽  
Vasoconstrictor Effect

Responses of pulmonary and systemic circulations of perinatal goats to prostaglandin F2α

1979 ◽  
Vol 57 (2) ◽  
pp. 167-173 ◽  
Author(s):  
Charles W. Leffler ◽  
Thom L. Tyler ◽  
Sidney Cassin
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Prostaglandin F2α ◽  
Systemic Circulation ◽  
Lower Sensitivity ◽  
Adrenergic Blockade ◽  
Premature Newborn ◽  
High Doses ◽  
Pressor Agent

The effects of exogenous prostaglandin (PG) F2α, as well as PGF1α and the 15-keto metabolites of both prostaglandins, upon unventilated fetal, premature newborn, and mature newborn goat pulmonary and systemic circulations were examined by infusing the compounds into the pulmonary circulation. PGF2α is a powerful pressor agent in both pulmonary and systemic circulations of fetal and neonatal goats. Broncho–pulmonary constriction was also observed in ventilated animals at infusion rates in excess of the lung's ability to catabolize the prostaglandin. The pressor effects were not attenuated by alpha-adrenergic blockade. PGF1α is qualitatively similar, but quantitatively less, in its effect. The 15-keto metabolites did not alter pulmonary or systemic circulation even at very high doses. The PGF2α threshold dose for increasing pulmonary vascular resistance is lowest in the unventilated fetus, greatest in the premature newborn, and intermediate in the newborn older than 1 day of age. The lower sensitivity of the pulmonary circulation to the exogenous vasoconstrictor in the immediate postventilation period suggests the presence of endogenous dilator activity. Since the increase in pulmonary vascular resistance produced by indomethacin is greatest in the newly ventilated fetus, less in the older newborn, and negligible in the unventilated fetus, the substance(s) responsible for the endogenous dilator activity would appear to require prostaglandin fatty acid cyclooxygenase activity for production.

Acute interaction of vasopressin and neurogenic mechanisms in DOC-salt hypertension

1982 ◽  
Vol 242 (1) ◽  
pp. H37-H43 ◽  
Author(s):  
H. Matsuguchi ◽  
P. G. Schmid
Keyword(s):  
Vascular Resistance ◽  
Arginine Vasopressin ◽  
Relative Role ◽  
Hypertensive Rats ◽  
Lumbar Sympathectomy ◽  
Vasopressin Antagonist ◽  
Salt Hypertension ◽  
And Control

We investigated the relative role of vasopressin and neurogenic factors in the control of vascular resistance in rats treated with desoxycorticosterone (DOC) and salt and in control rats. DOC-salt-treated rats had elevated hindquarter vascular resistance (P less than 0.05). Vasopressin and neurogenic tone contributed significantly (P less than 0.05) to increased resistance. Vasodilator responses to a specific vasopressin antagonist, I-deaminopenicillamine, 4-valine, 8-D-arginine vasopressin (dPVDAVP), and lumbar sympathectomy in separate DOC-salt groups accounted for 40 +/- 5 (SE) and 43 +/- 6%, respectively, of the total vasodilator capacity. In contrast, corresponding responses to dPVDAVP and lumbar sympathectomy in control rats were smaller (P less than 0.01), were significantly different (P less than 0.05), and accounted for 8 +/- 3 and 20 +/- 3%, respectively, of the total vasodilator capacity. Effects of dPVDAVP compared in innervated hindquarters of DOC-salt-treated and control rats were greater in DOC-salt-treated rats (P less than 0.001); in the denervated hindquarters the effects of dPVDAVP were similar in DOC-salt-treated and control rats. Therefore, effects of vasopressin on vascular resistance were augmented in DOC-salt-treated hypertensive rats; furthermore this augmented effect was dependent on an intact innervation.

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