Assessment of Autonomic and Non-Autonomic Components of Resting Hindlimb Vascular Resistance and Reactivity to Pressor Substances in Renal Hypertensive Rabbits

1976 ◽  
Vol 51 (s3) ◽  
pp. 57s-59s
Author(s):  
J. A. Angus ◽  
M. J. West ◽  
P. I. Korner
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Structural Changes ◽  
Resistance Vessels ◽  
Structural Differences ◽  
Before And After ◽  
Autonomic Blockade ◽  
Autonomic Component

1. Hindlimb vascular resistance (HVR) was measured before and after pharmacological autonomic blockade in unanaesthetized renal cellophan-wrap hypertensive or normotensive rabbits with previously implanted Doppler ultrasonic flowmeters. 2. When the blood pressure was restored to resting values after autonomic block, the elevated resting HVR in the hypertensive rabbits was entirely accounted for by an increased non-autonomic component (i.e. HVR after block). If the pressure was not restored after block the autonomic component (i.e. resting HVR minus non-autonomic HVR) was overestimated and the non-autonomic component was underestimated. 3. During maximum vasodilatation the minimum HVR was significantly higher in the hypertensive rabbits than in the normotensive group, probably due to structural differences of resistance vessels. 4. Reactivity of the hindlimb bed to noradrenaline, angiotensin II and vasopressin injections was approximately twice as great in the hypertensive rabbits as in the sham-operated group, probably as a consequence of the structural changes.

Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism

1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Cardiac Output ◽  
No Synthase ◽  
Before And After ◽  
Regional Hemodynamics ◽  
Autonomic Blockade ◽  
Infusion Of Norepinephrine ◽  
Oxide Synthase

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.

scholarly journals PERAN KOMPLEKS JUKSTAGLOMERULUS TERHADAP RESISTENSI PEMBULUH DARAH

2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Renny M. Toreh ◽  
Sonny J.R. Kalangi ◽  
Sunny Wangko
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Sodium Intake ◽  
Angiotensin Receptor Blockers ◽  
Antihypertensive Agents ◽  
Angiotensin I ◽  
Renin Angiotensin ◽  
Renin Synthesis ◽  
Receptor Blockers

Abstract: As the main structural component of the renin-angiotensin-aldosterone system (RAAS), the juxtaglomerular complex plays a very important role in the regulation of vascular resistance. The synthesis and release of renin into the circulation occurs due to the decrease of blood pressure, loss of body fluid, and a decrease of sodium intake. Renin converts angiotensinogen into angiotensin I, which is further converted by the angiotensin converting enzyme (ACE) into angiotensin II. This angiotensin II causes vasoconstriction of blood vessels, resulting in an increase of vascular resistance and blood pressure. The ACE inhibitors and the angiotensin receptor blockers (ARBs) do not inhibit the RAAS completely since they cause an increase of renin activity. The renin blockers are more effective in inhibiting RAAS activity; therefore, these renin blockers can be applied as antihypertensive agents with fewer side effects. The RAAS activity can be inhibited by a decrease of renin synthesis in the juxtaglomerular complex by blocking the signals in the juxtaglomerular complex that stimulate renin synthesis, and by blocking the gap junctions in the juxtaglomerular complex. Keywords: juxtaglomerular complex, vascular resistance, RAAS.   Abstrak: Kompleks jukstaglomerulus sebagai komponen struktural utama sistem renin angiotensin berperan penting dalam pengaturan resistensi pembuluh darah. Sintesis dan pelepasan renin ke sirkulasi terjadi karena tekanan darah yang rendah, kehilangan cairan tubuh, dan kurangnya intake natrium. Renin akan memecah angiotensinogen menjadi angiotesin I yang kemudian secara cepat dikonversi oleh enzim pengonversi angiotensin  menjadi angiotensin II. Angiotensin II menyebabkan vasokontriksi pembuluh darah sehingga meningkatkan resistensi pembuluh darah yang pada akhirnya akan meningkatkan tekanan darah. ACEinhibitor dan ARB kurang sempurna dalam menghambat kerja SRAA oleh karena keduanya memutuskan rantai mekanisme timbal balik sehingga meningkatkan aktifitas renin. Penghambat renin lebih efektif digunakan untuk menghambat aktifitas SRAA sehingga penghambat renin dapat digunakan sebagai obat anti-hipertensi dan memiliki efek samping yang rendah. Metode penghambatan SRAA yang juga dapat dikembangkan ialah penghambatan sintesis renin dalam kompleks jukstaglomerulus dengan cara menekan sinyal-sinyal dalam kompleks jukstaglomerulus yang merangsang sintesis renin dan menghambat fungsi taut kedap yang terdapat dalam kompleks jukstaglomerulus. Kata kunci: kompleks juksta glomerulus, resistensi vaskular, SRAA.

Endothelin antagonist reduces hemodynamic responses to vasopressin in DOCA-salt hypertension

2001 ◽  
Vol 281 (6) ◽  
pp. H2511-H2517 ◽  
Author(s):  
Ming Yu ◽  
Venkat Gopalakrishnan ◽  
Thomas W. Wilson ◽  
J. Robert McNeill
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Hemodynamic Responses ◽  
Hypertensive Group ◽  
Time Flow ◽  
Before And After ◽  
Vascular Responsiveness

The contribution of endothelin to the changes in blood pressure, cardiac output, and total peripheral resistance evoked by arginine vasopressin and angiotensin II was investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by infusing the peptides intravenously before and after pretreatment with the endothelin receptor antagonist bosentan. Blood pressure was recorded with radiotelemetry devices and cardiac output was recorded with ultrasonic transit time flow probes in conscious unrestrained animals. The dose-related decreases in cardiac output induced by vasopressin and angiotensin II were unaffected by bosentan. In contrast, the dose-related increases in total peripheral resistance evoked by vasopressin were blunted in both DOCA-salt hypertensive and sham normotensive rats, but this effect of bosentan was greater in the DOCA-salt hypertensive group. In contrast with vasopressin, bosentan failed to change hemodynamic responses to angiotensin II. The exaggerated vascular responsiveness (total peripheral resistance) of the DOCA-salt hypertensive group to vasopressin was largely abolished by bosentan. These results suggest that endothelin contributes to the hemodynamic effects of vasopressin but not angiotensin II in the DOCA-salt model of hypertension.

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.

scholarly journals Attenuation of hypertension-mediated glomerulosclerosis in conjunction with increased angiotensin (1–7)

2011 ◽  
Vol 5 (6) ◽  
pp. 297-304 ◽  
Author(s):  
Michiya Igase ◽  
Hiroshi Yokoyama ◽  
Carlos M. Ferrario
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Structural Changes ◽  
Weight Ratio ◽  
Critical Factor ◽  
Vehicle Group ◽  
Glomerular Sclerosis ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor ◽  
Hypertensive Nephropathy

Background: Controversy exists as to whether angiotensin (1–7) (Ang (1–7)) acts as a protective hormone against renal injury. Methods: We compared the degree of improvement of hypertensive nephropathy following 8 weeks’ treatment with either the angiotensin II receptor type 1 antagonist olmesartan medoxomil or the cardioselective beta blocker atenolol in 8-week-old spontaneously hypertensive rats (SHRs). Results: Both treatment regimens reduced mean blood pressure in a similar fashion, while bradycardia was present only in atenolol-treated SHRs. The heart weight:body weight ratio fell more in SHRs medicated with olmesartan versus those receiving atenolol. These changes were associated with increases in plasma Ang II in SHRs given the angiotensin II receptor blocker. At the end of treatment, plasma Ang (1–7) was higher in the olmesartan than atenolol or vehicle groups. The glomerular sclerosis (GS) index was lowered by olmesartan and atenolol compared with the vehicle group. While both olmesartan and atenolol attenuated renal perivascular collagen deposition (PVCD), the greatest effect was observed in SHRs receiving olmesartan. Elevations in plasma Ang (1–7) correlated negatively with reductions in GS or PVCD index, respectively. Conclusions: While control of blood pressure remains a critical factor in the prevention of hypertensive nephropathy, Ang (1–7) may play a substantial role in preventing the structural changes in glomerulus through its effect on regulations of blood pressure and renal function.

EFFECTS OF PROSTAGLANDIN F2α ON OVARIAN BLOOD FLOW AND VASCULAR RESISTANCE IN THE PSEUDOPREGNANT RABBIT

1975 ◽  
Vol 79 (2) ◽  
pp. 337-350 ◽  
Author(s):  
Per Olof Janson ◽  
Ivan Albrecht ◽  
Kurt Ahrén
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Prostaglandin F2α ◽  
Interstitial Tissue ◽  
Corpora Lutea ◽  
Luteal Function ◽  
Direct Measurements ◽  
Before And After

ABSTRACT In the search for data supporting the hypothesis that the luteolytic effect of prostaglandins (PG) is initiated by a vascular mechanism, some haemodynamic parameters including ovarian blood flow and vascular resistance were measured in pseudopregnant anaesthetized rabbits before and after exogenous administration of PGF2α. The measurements were performed on days 5–10 of pseudopregnancy induced by 500 IU HCG iv. Infusion of 50 μg/kg PGF2α iv over a one-minute period caused significant falls in cardiac output, heart rate and blood pressure after 1–3 min. Blood pressure and cardiac output were normalized after 16–49 min. Blood flow in the ovarian vein (direct measurements) decreased and returned to initial values parallel to the blood pressure and no change in resistance in the vascular bed drained by the vein was noted. Total ovarian blood flow and resistance, as measured in surgically intact ovaries before and after PG infusion, using 35 or 15 μm 169Yb and 46Sc-labelled microspheres, changed and remained constant respectively, according to the same pattern as in the direct measurements. The distribution of blood flow between the corpora lutea and the interstitial tissue of the ovary measured by 15 μm radioactive microspheres. PGF2α caused an interstitial vasodilation whereas no significant change in luteal vascular resistance was noted. Since luteal blood flow represented a predominant part of total ovarian flow in the type of ovary studied, the interstitial vasodilatation caused only negligible changes in blood flow to the whole ovary. The present study does not support the hypothesis of a PG-induced luteal blood flow reduction preceding luteolysis. The possible significance of the interstitial vasodilatation for luteal function remains to be elucidated.

Cardiopulmonary reflexes and blood pressure in exercising sinoaortic-denervated dogs

1984 ◽  
Vol 57 (5) ◽  
pp. 1417-1421 ◽  
Author(s):  
D. A. Daskalopoulos ◽  
J. T. Shepherd ◽  
S. C. Walgenbach
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vagal Afferents ◽  
Systemic Resistance ◽  
Vigorous Exercise ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Cardiopulmonary Receptors

To examine the role of cardiopulmonary receptors in arterial blood pressure regulation during and after exercise, conscious dogs with chronic sinoaortic denervation were subjected to 12 min of light exercise and 12 min of exercise that increased in severity every 3 min. Hemodynamic measurements were made before and after interruption of cardiopulmonary afferents by bilateral cervical vagotomy. During both exercise protocols, after an initial transient decrease, the arterial blood pressure remained close to resting values before and after vagotomy. On cessation of the graded exercise, the arterial blood pressure did not change before, but a rapid and sustained increase in pressure occurred after vagotomy. At the time of this increase the cardiac output and heart rate were returning rapidly to the resting level. The study demonstrates that in the chronic absence of arterial baroreflexes, vagal afferents prevent a rise in arterial blood pressure after vigorous exercise presumably by the action of cardiopulmonary receptors causing a rapid dilatation of systemic resistance vessels.

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

Critical opening pressure and reactivity of tail vessels in conscious hypertensive rats

1976 ◽  
Vol 54 (3) ◽  
pp. 314-321
Author(s):  
A. C. Darke ◽  
P. G. Nair ◽  
P. Gaskell
Keyword(s):  
Blood Pressure ◽  
Renovascular Hypertension ◽  
Vascular Reactivity ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Opening Pressure ◽  
Critical Opening ◽  
Resistance Vessels ◽  
Before And After ◽  
Desoxycorticosterone Acetate

The possible role of increased vascular reactivity in the mechanism of experimental hypertension was studied by measurements of the critical opening pressure (COP) of tail vessels in conscious rats. In hypertension induced by administration of desoxycorticosterone acetate (DOCA) and replacement of the drinking water by 1% NaCl solution (DOCA–NaCl hypertension), and in one-kidney Goldblatt renovascular hypertension, the raised level of blood pressure was associated with an increased COP of the tail vessels when measured both before and after ganglionic blockade. In rats treated with either DOCA alone or 1% NaCl alone there was no significant increase in systolic blood pressure (SBP) or COP relative to the corresponding controls. In all four experimental series intravenous infusion of angiotensin or norepinephrine in conscious ganglion-blocked rats produced dose-dependent increases in SBP and COP. In DOCA–NaCl hypertensive rats but not in renovascular hypertensives, nor in rats treated with DOCA alone or 1% NaCl alone, the increase in COP for a given increment in dose of angiotensin or norepinephrine was significantly greater than in the control rats. It is concluded that in DOCA–NaCl hypertension there is a true increase in the reactivity of the smooth muscle of the resistance vessels to angiotensin and norepinephrine. In renovascular hypertension this is not the case and other factors must therefore be involved in causing the increased blood pressure and COP.

Effect of [Sar1, Ala8]-angiotensin II and hypophysectomy on the intestinal resistance vessels and blood pressure following furosemide-induced volume depletion

1976 ◽  
Vol 54 (3) ◽  
pp. 373-380 ◽  
Author(s):  
J. Robert McNeill ◽  
William C. Wilcox ◽  
Raoul Regnault
Keyword(s):  
Blood Pressure ◽  
Control System ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Adrenal Glands ◽  
The Other ◽  
Volume Depletion ◽  
Competitive Antagonist ◽  
Vasoconstrictor Response ◽  
Resistance Vessels

Intravenous administration of furosemide (2 mg/kg) caused intestinal vasoconstriction in various groups of pentobarbital-anesthetized cats. [Sar1, Ala8]-angiotensin II, a specific competitive antagonist of angiotensin II, was infused 60 min after administration of furosemide, a time when the intestinal vasoconstrictor response to the diuretic was maximal or near maximal. In hypophysectomized animals, infusion of the antagonist abolished the intestinal vasoconstriction and caused a significant fall in arterial pressure even when the intestinal nerves and adrenal glands remained intact. In contrast, the antagonist had little effect when the pituitary gland remained intact. The results suggest that endogenous angiotensin and vasopressin are overlapping mechanisms which constrict the intestinal resistance vessels and support arterial pressure following furosemide-induced volume depletion. In the absence of one control system, the other compensates to maintain the responses.

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