Vestibular stimulation leads to distinct hemodynamic patterning

Previous studies demonstrated that responses of a particular sympathetic nerve to vestibular stimulation depend on the type of tissue the nerve innervates as well as its anatomic location. In the present study, we sought to determine whether such precise patterning of vestibulosympathetic reflexes could lead to specific hemodynamic alterations in response to vestibular afferent activation. We simultaneously measured changes in systemic blood pressure and blood flow (with the use of Doppler flowmetry) to the hindlimb (femoral artery), forelimb (brachial artery), and kidney (renal artery) in chloralose-urethane-anesthetized, baroreceptor-denervated cats. Electrical vestibular stimulation led to depressor responses, 8 ± 2 mmHg (mean ± SE) in magnitude, that were accompanied by decreases in femoral vasoconstriction (23 ± 4% decrease in vascular resistance or 36 ± 7% increase in vascular conductance) and increases in brachial vascular tone (resistance increase of 10 ± 6% and conductance decrease of 11 ± 4%). Relatively small changes (<5%) in renal vascular tone were observed. In contrast, electrical stimulation of muscle and cutaneous afferents produced pressor responses (20 ± 6 mmHg) that were accompanied by vasoconstriction in all three beds. These data suggest that vestibular inputs lead to a complex pattern of cardiovascular changes that is distinct from that which occurs in response to activation of other types of somatic afferents.

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Stimulation of renin release by prostaglandin E2 is mediated by EP2 and EP4 receptors in mouse kidneys

AJP Renal Physiology ◽

10.1152/ajprenal.00072.2004 ◽

2004 ◽

Vol 287 (3) ◽

pp. F427-F433 ◽

Cited By ~ 71

Author(s):

Frank Schweda ◽

Jürgen Klar ◽

Shuh Narumiya ◽

Rolf M. Nüsing ◽

Armin Kurtz

Keyword(s):

Vascular Tone ◽

Threshold Concentration ◽

Renin Release ◽

Receptor Subtypes ◽

Wild Type ◽

Adrenoceptor Agonist ◽

Functional Relevance ◽

Renal Vascular ◽

Renal Vascular Tone ◽

Stimulation Of

PGE2 is a potent stimulator of renin release. So far, the contribution of each of the four PGE2 receptor subtypes (EP1–EP4) in the regulation of renin release has not been characterized. Therefore, we investigated the effects PGE2 on renin secretion rates (RSR) from isolated, perfused kidneys of EP1−/−, EP2−/−, EP3−/−, EP4−/−, and wild-type mice. PGE2 concentration dependently stimulated RSR from kidneys of all four knockout strains with a threshold concentration of 1 nM in EP1−/−, EP2−/−, EP3−/−, and wild-type mice, whereas the threshold concentration was shifted to 10 nM in EP4−/− mice. Moreover, the maximum stimulation of RSR by PGE2 at 1 μM was significantly reduced in EP4−/− (12.8-fold of control) and EP2−/− (15.9-fold) compared with wild-type (20.7-fold), EP1−/− (23.8-fold), and EP3−/− (20.1-fold). In contrast, stimulation of RSR by either the loop diuretic bumetanide or the β-adrenoceptor agonist isoproterenol was similar in all strains. PGE2 exerted a dual effect on renal vascular tone, inducing vasodilatation at low concentrations (1 nmol/) and vasoconstriction at higher concentrations (100 nmol/) in kidneys of wild-type mice. In kidneys of EP2−/− as well as EP4−/− mice, vasodilatation at low PGE2 concentrations was prevented, whereas vasoconstriction at higher concentrations was augmented. In contrast, the vasodilatatory component was pronounced in kidneys of EP1 and EP3 knockout mice, whereas in both genotypes the vasoconstriction at higher PGE2 concentrations was markedly blunted. Our data provide evidence that PGE2 stimulates renin release via activation of EP2 and EP4 receptors, whereas EP1 and EP3 receptors appear to be without functional relevance in juxtaglomerular cells. In contrast, all four receptor subtypes are involved in the control of renal vascular tone, EP1 and EP3 receptors increasing, and EP2 as well as EP4 receptors, decreasing it.

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Mechanisms of pressor response produced by stimulation of nucleus ambiguus

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.259.5.r955 ◽

1990 ◽

Vol 259 (5) ◽

pp. R955-R962

Author(s):

B. H. Machado ◽

M. J. Brody

Keyword(s):

Arterial Pressure ◽

Vascular Resistance ◽

Pressor Response ◽

Nucleus Ambiguus ◽

Ventrolateral Medulla ◽

Pressor Responses ◽

Regional Vascular Resistance ◽

Parasympathetic Control ◽

Renal Vascular ◽

Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

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Effect of Captopril on Renal Vascular Tone in Patients with Essential Hypertension

Clinical Science ◽

10.1042/cs057421s ◽

1979 ◽

Vol 57 (s5) ◽

pp. 421s-423s ◽

Cited By ~ 47

Author(s):

A. Mimran ◽

H. R. Brunner ◽

G. A. Turini ◽

B. Waeber ◽

D. Brunner

Keyword(s):

Essential Hypertension ◽

Vascular Tone ◽

Sodium Intake ◽

Renal Plasma Flow ◽

Sodium Diet ◽

Low Sodium Diet ◽

Low Sodium ◽

Urinary Potassium ◽

Renal Vascular ◽

Renal Vascular Tone

1. The effect of acute inhibition of angiotensin-converting enzyme by captopril (50 mg) on renal haemodynamics and function was assessed in nine patients with essential hypertension on unrestricted sodium intake (n = 8) or low sodium diet (n = 1). 2. Captopril induced a rapid and significant decrease in arterial pressure, which was maximal within 60 min. 3. Effective renal plasma flow (ERPF) increased, glomerular filtration rate (GFR) did not change and filtration fraction (FF) decreased after captopril. No change in sodium excretion and a decrease in urinary potassium occurred. 4. In the patient on low sodium diet, captopril induced striking increases in GFR and ERPF (64 and 106% respectively). 5. The logarithm of baseline plasma renin activity was positively correlated with the change in ERPF and negatively correlated with changes in FF and renal resistance. 6. The results indicate that in patients with essential hypertension angiotensin participates actvely in the maintenance of renal vascular tone at the efferent arteriolar level. A possible influence of kinins remains to be defined.

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Interactions Between Neural and Hormonal Mediators of Renal Vascular Tone in Anaesthetized Rabbits

Experimental Physiology ◽

10.1113/eph8802462 ◽

2003 ◽

Vol 88 (2) ◽

pp. 229-241 ◽

Cited By ~ 23

Author(s):

Sarah-Jane Guild ◽

Carolyn J. Barrett ◽

Roger G. Evans ◽

Simon C. Malpas

Keyword(s):

Vascular Tone ◽

Renal Vascular ◽

Renal Vascular Tone

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Contribution of endothelin to renal vascular tone and autoregulation in the conscious dog

AJP Renal Physiology ◽

10.1152/ajprenal.1999.276.3.f417 ◽

1999 ◽

Vol 276 (3) ◽

pp. F417-F424 ◽

Cited By ~ 9

Author(s):

Heike Berthold ◽

Klaus Münter ◽

Armin Just ◽

Hartmut R. Kirchheim ◽

Heimo Ehmke

Keyword(s):

Time Course ◽

Vascular Tone ◽

Ace Inhibition ◽

Renal Hemodynamics ◽

Receptor Subtype ◽

Ang Ii ◽

Renal Autoregulation ◽

Arterial Blood ◽

Renal Vascular ◽

Renal Vascular Tone

Exogenous endothelin-1 (ET-1) is a strong vasoconstrictor in the canine kidney and causes a decrease in renal blood flow (RBF) by stimulating the ETA receptor subtype. The aim of the present study was to investigate the role of endogenously generated ET-1 in renal hemodynamics under physiological conditions. In six conscious foxhounds, the time course of the effects of the selective ETA receptor antagonist LU-135252 (10 mg/kg iv) on mean arterial blood pressure (MAP), heart rate (HR), RBF, and glomerular filtration rate (GFR), as well as its effects on renal autoregulation, were examined. LU-135252 increased RBF by 20% (from 270 ± 21 to 323 ± 41 ml/min, P < 0.05) and HR from 76 ± 5 to 97 ± 8 beats/min ( P< 0.05), but did not alter MAP, GFR, or autoregulation of RBF and GFR. Since a number of interactions between ET-1 and the renin-angiotensin system have been reported previously, experiments were repeated during angiotensin converting enzyme (ACE) inhibition by trandolaprilat (2 mg/kg iv). When ETA receptor blockade was combined with ACE inhibition, which by itself had no effects on renal hemodynamics, marked changes were observed: MAP decreased from 91 ± 4 to 80 ± 5 mmHg ( P < 0.05), HR increased from 85 ± 5 to 102 ± 11 beats/min ( P < 0.05), and RBF increased from 278 ± 23 to 412 ± 45 ml/min ( P< 0.05). Despite a pronounced decrease in renal vascular resistance over the entire pressure range investigated (40–100 mmHg), the capacity of the kidneys to autoregulate RBF was not impaired. The GFR remained completely unaffected at all pressure levels. These results demonstrate that endogenously generated ET-1 contributes significantly to renal vascular tone but does not interfere with the mechanisms of renal autoregulation. If ETAreceptors are blocked, then the vasoconstrictor effects of ET-1 in the kidney are compensated for to a large extent by an augmented influence of ANG II. Thus ET-1 and ANG II appear to constitute a major interrelated vasoconstrictor system in the control of RBF.

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Physiological and pathophysiological roles of oxygen radicals in the renal microvasculature

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00605.2001 ◽

2002 ◽

Vol 282 (2) ◽

pp. R335-R342 ◽

Cited By ~ 116

Author(s):

Christine G. Schnackenberg

Keyword(s):

Diabetes Mellitus ◽

Oxygen Radicals ◽

Vascular Tone ◽

Tubuloglomerular Feedback ◽

Normal Kidney ◽

Renal Vasoconstriction ◽

Increased Sensitivity ◽

Renal Microvasculature ◽

Renal Vascular ◽

Renal Vascular Tone

The renal microvasculature is an important component in the regulation of kidney function. Recent studies suggest that oxygen radicals can contribute to the modulation of renal cortical and medullary microvascular function under normal conditions as well as in pathophysiological conditions such as diabetes mellitus and hypertension. This review focuses on studies that indicate oxygen radicals can cause renal vasoconstriction, mediate the vasoconstriction of other agonists, and modulate nitric oxide-dependent actions in the normal kidney. Hypertension and diabetes mellitus are associated with oxidative stress. Recent investigations suggest that oxygen radicals may contribute to the enhanced renal vascular tone, increased sensitivity to vasoconstrictors, impaired endothelium-dependent vasodilation, and enhanced tubuloglomerular feedback found in these pathophysiological conditions.

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The Effect of Electrical Stimulation of the Pudendal Nerve on Sciatic Nerve Blood Flow in Animals

Acupuncture in Medicine ◽

10.1136/aim.26.3.145 ◽

2008 ◽

Vol 26 (3) ◽

pp. 145-148 ◽

Cited By ~ 7

Author(s):

Motohiro Inoue ◽

Tatsuya Hojo ◽

Miwa Nakajima ◽

Hiroshi Kitakoji ◽

Megumi Itoi ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Electrical Stimulation ◽

Sciatic Nerve ◽

Pudendal Nerve ◽

Systemic Blood Pressure ◽

Nerve Blood Flow ◽

Doppler Flowmetry ◽

Canal Stenosis ◽

Stimulation Of

Objective To investigate the mechanism of the clinical effect of electroacupuncture of the pudendal nerve on the lumbar and lower limb symptoms caused by lumbar spinal canal stenosis, we studied changes in sciatic nerve blood flow during electrical stimulation of the pudendal nerve in the rat. Methods Using rats (n=5), efferent electrical stimulation to the pudendal nerve was performed and sciatic nerve blood flow was measured with laser Doppler flowmetry. Simultaneously, changes in the blood pressure and cardiac rate were measured. Furthermore, the effect of atropine on these responses to the stimulation was also studied. Results Electrical stimulation of the pudendal nerve significantly increased blood flow in the sciatic nerve transiently without increasing heart rate and systemic blood pressure. The significant increase in the sciatic nerve blood flow disappeared after administration of atropine. Conclusion Electrical stimulation of the pudendal nerve causes a transient and significant increase in sciatic nerve blood flow. This response is eliminated or attenuated by administration of atropine, indicating that it occurs mainly via cholinergic nerves.

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Renovascular BKCa channels are not activated in vivo under resting conditions and during agonist stimulation

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00337.2006 ◽

2007 ◽

Vol 292 (1) ◽

pp. R345-R353 ◽

Cited By ~ 16

Author(s):

Linda Magnusson ◽

Charlotte Mehlin Sorensen ◽

Thomas Hartig Braunstein ◽

Niels-Henrik Holstein-Rathlou ◽

Max Salomonsson

Keyword(s):

Vascular Tone ◽

Ang Ii ◽

Small Reduction ◽

Bkca Channels ◽

Agonist Stimulation ◽

Electromagnetic Flowmetry ◽

Renal Vascular ◽

Renal Vascular Tone

We investigated the role of large-conductance Ca2+-activated K+ (BKCa) channels for the basal renal vascular tone in vivo. Furthermore, the possible buffering by BKCa of the vasoconstriction elicited by angiotensin II (ANG II) or norepinephrine (NE) was investigated. The possible activation of renal vascular BKCa channels by cAMP was investigated by infusing forskolin. Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry or ultrasonic Doppler. Renal preinfusion of tetraethylammonium (TEA; 3.0 μmol/min) caused a small reduction of baseline RBF, but iberiotoxin (IBT; 0.3 nmol/min) did not have any effect. Renal injection of ANG II (1–4 ng) or NE (10–40 ng) produced a transient decrease in RBF. These responses were not affected by preinfusion of TEA or IBT. Renal infusion of the BKCa opener NS-1619 (90.0 nmol/min) did not affect basal RBF or the response to NE, but it attenuated the response to ANG II. Coadministration of NS-1619 with TEA or IBT abolished this effect. Forskolin caused renal vasodilation that was not inhibited by IBT. The presence of BKCa channels in the preglomerular vessels was confirmed by immunohistochemistry. Despite their presence, there is no indication for a major role for BKCa channels in the control of basal renal tone in vivo. Furthermore, BKCa channels do not have a buffering effect on the rat renal vascular responses to ANG II and NE. The fact that NS-1619 attenuates the ANG II response indicates that the renal vascular BKCa channels can be activated under certain conditions.

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Cardiovascular Effects of Prazosin in Dogs

Clinical Science ◽

10.1042/cs051609s ◽

1976 ◽

Vol 51 (s3) ◽

pp. 609s-612s ◽

Cited By ~ 2

Author(s):

I. Cavero

Keyword(s):

Vascular Tone ◽

Pressor Response ◽

Cardiovascular Effects ◽

Acute Administration ◽

Experimental Conditions ◽

Bilateral Carotid Occlusion ◽

Pressor Responses ◽

Bilateral Carotid ◽

Aortic Blood Pressure ◽

Stimulation Of

1. In pentobarbitone-anaesthetized dogs, prazosin (2×1·3 μmol day—1 kg—1; 2×0·5 mg day—1 kg—1) administered orally for 3 days reduced resting aortic blood pressure as well as the pressor response to bilateral carotid occlusion. Prazosin neither affected resting heart rate nor the tachycardia induced by intravenous isoprenaline, noradrenaline and electrical stimulation of preganglionic and postganglionic sympathetic nerve fibres. Prazosin significantly attenuated the fall in perfusion pressure in a perfused hind leg resulting from the section of the ipsilateral sympathetic lumbar chain. Furthermore, the drug inhibited by about 50% the hind-leg pressor responses elicited by intra-arterial administration of α-adrenoreceptor agonists and by stimulation of the lumbar sympathetic chain, without altering the effects of angiotensin II. 2. Acute administration of prazosin into the innervated hind leg provoked a dose-related reduction in vascular resistance. However, after spinal anaesthesia no such an effect was observed even when vascular tone was increased by infusion of vasopressin. Under the same experimental conditions administration of papaverine induced a vasodilatation. 3. This study confirms that prazosin impairs the function of vascular α-adrenoreceptors, and strongly challenges the claim that this compound produces a directly mediated vasodilatation of the leg vascular bed.

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