scholarly journals The role of l-type calcium channels in the mediation of fast oscillation of arterial blood pressure and renal blood flow in rats

2019 ◽  
Vol 17 (3) ◽  
pp. 253-258
Author(s):  
P. Markova ◽  
R. Girchev
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Experimental Period ◽  
Doppler Probe ◽  
Arterial Blood ◽  
Male Wistar Rats ◽  
Ca2 Channels

The investigation of dynamic characteristics of blood pressure and renal blood flow provides detailed information about the fast regulatory mechanisms involved in arterial blood pressure (ABP) and renal blood flow (RBF) autoregulation. The aim of our study was to investigate the role of L-type Ca2+ channels in the mediation of fast oscillations of arterial blood pressure and renal blood flow in rats by means of spectral analysis. The experiments were performed on anesthetized male Wistar rats (n=7) at the age of 12-14 weeks. The ABP was measured directly in femoral artery; RBF was registered by perivascular ultrasonic Doppler probe (Transonic system) in control and experimental period. The spectrograms from APB and RBF were derived in Lab View 3.11 software. In experimental period the selective L-type Ca2+ channel blocker amlodipine besylate (AML) in dose 200 mkg.kg-1 bolus followed by 50 mkg.kg-1.h infusions was applied. Our results by using a spectral method of analysis of ABP and RBF confirmed involvement of L-type Ca2+ channels in the mediation of dynamic nature of myogenic vascular response. The L-type Ca2+ channels in different specific manner participate in the regulation of renal blood flow and arterial blood pressure.

Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Arginine Infusion ◽  
Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

Abstract 1785: Renal Artery Angioplasty Improves Diastolic Cardiac Function In Patients With heart failure Possessing Renal Artery Stenosis.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Eisei Yamamoto ◽  
Hitoshi Takano ◽  
Hiroyuki Tajima ◽  
Jun Tanabe ◽  
Hidekazu Kawanaka ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Function ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Renal Artery Stenosis ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Diastolic Cardiac Function

Background: Renal artery stenosis (RAS) often plays an important role not only in malignant hypertension but also in sudden development of heart failure (HF) so called ‘flash pulmonary edema’ or chronic HF refractory to medical treatment. One of the possible mechanisms whereby RAS affects these unique conditions of HF is suppression of LV compliance through the complex interaction between neurohormonal systems originating from the reduction of renal blood flow. Renal artery angioplasty is expected to be an effective treatment for restoring renal blood flow in patients with RAS. The aim of the present study was whether the angioplasty can improve the impaired neurohormonal systems and diastolic cardiac function in patients with RAS. Methods: A prospective analysis was performed in 18 HF patients with RAS (age: 72±6, 3 females, NYHA I/II/III: 5/9/4) who underwent renal artery angioplasty between 2005 and 2007. Four patients with significant bilateral RAS and 3 patients with unilateral RAS in the vessel supplying a functional solitary kidney were included. We monitored the changes of biochemical and neurohormonal markers and blood pressure. Cardiac function was evaluated by tissue Doppler echocardiogram before and 3 months after the procedure. Results: Technical success was achieved in all interventions. The results are shown in table . Systolic arterial blood pressure significantly decreased by renal angioplasty. B-type natriuretic peptide (BNP) was significantly reduced 3 months after the angioplasty, whereas the change of sCr or angiotensinII was not statistically significant. Myocardial early diastolic velocity (Em), a parameter of diastolic LV function, was significantly improved compared with that measured before the procedure. Conclusions: In patients with either overt or latent HF possessing RAS, renal artery angioplasty not only decreases arterial blood pressure but also improves diastolic cardiac function in parallel with the reduction of BNP level.

Autoregulation of Renal Blood Flow in Dogs at Normal Body Temperature and at 27°C

1975 ◽  
Vol 48 (6) ◽  
pp. 501-508 ◽  
Author(s):  
B. J. Chapman ◽  
W. R. Withey ◽  
K. A. Munday
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Vasculature ◽  
Normal Body Temperature ◽  
Arterial Blood ◽  
Two Temperatures ◽  
The Mean

1. Dogs cooled to 27°C were compared with control dogs maintained at 38°C. The mean arterial blood pressure, renal blood flow and glomerular filtration rate were lower in the hypothermic animals. 2. The relation between mean arterial blood pressure and renal blood flow was investigated. Autoregulation of renal blood flow occurred in the kidneys of normothermic and hypothermic animals. Thus the reduction in renal blood flow during hypothermia is not due simply to the fall in mean arterial blood pressure. 3. Similarities between recordings of renal blood flow obtained at 38°C and 27°C suggest that its autoregulation occurs by the same mechanism at the two temperatures. 4. Autoregulation of renal blood flow occurred in hypothermic kidneys in the presence of a cold-induced vasoconstriction. The observed responses to cold and to alterations in mean arterial blood pressure may take place in different areas of the renal vasculature.

Renal vascular effects of epinephrine infusion in the halothane-anesthetized piglet

1994 ◽  
Vol 72 (4) ◽  
pp. 394-396 ◽  
Author(s):  
Keith J. Harrington ◽  
Robert G. Allen ◽  
Jay W. Dewald
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Renal Vascular Resistance ◽  
Epinephrine Infusion ◽  
Arterial Blood ◽  
Renal Vascular

The objective of this study was to determine the dose–response effects of epinephrine, given by systemic intravenous infusion to the halothane-anesthetized newborn piglet, on renal blood flow, mean arterial blood pressure, and renal vascular resistance. Seven newborn piglets were acutely instrumented. A transit-time ultrasound flow probe was placed around the renal artery and a femoral arterial catheter was placed for blood pressure monitoring. Epinephrine was infused in doubling doses from 0.2 to 3.2 μg∙kg−1∙min−1. Mean arterial blood pressure increased from 54 mmHg (1 mmHg = 133.3 Pa) to an average of 96 mmHg at 3.2 μg∙kg−1∙min−1 of epinephrine. Renal blood flow increased from 165 mL∙min−1∙100 g−1 at baseline to 185 mL∙min−1∙100 g−1 at a dose of 0.2 μg∙kg−1∙min−1 and increased further at 0.4 and 0.8 μg∙kg−1∙min−1 to reach 261 mL∙min−1∙100 g−1. Renal blood flow began to fall at a dose of 3.2 μg∙kg−1∙min−1, remaining however, significantly above baseline (211 mL∙min−1∙100 g−1). Consequently, calculated renal vascular resistance fell as the dose was increased from 0.2 to 0.8 μg∙kg−1∙min−1 and then rose again at 1.6 and 3.2 μg∙kg−1∙min−1, being significantly above baseline at 3.2 μg∙kg−1∙min−1. These results demonstrate that epinephrine when given by systemic infusion to the halothane-anesthetized newborn pig is a renal vasodilator at low doses and causes renal vasoconstriction at moderate to high doses. Renal blood flow remained above baseline at all doses tested, and thus, within the dosage range tested, epinephrine infusion should not cause renal ischemia.Key words: epinephrine, kidney blood flow, piglet, renal vascular resistance.

Renal and iliac vascular responses to left ventricular receptor stimulation in conscious dogs

1984 ◽  
Vol 246 (5) ◽  
pp. R788-R798
Author(s):  
A. J. Gorman ◽  
K. G. Cornish ◽  
I. H. Zucker
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Neural Control ◽  
Cholinergic Receptor ◽  
Left Ventricular ◽  
Conscious Dog ◽  
Arterial Blood

The purpose of the present study was to investigate the relative responses of the renal and iliac vascular beds to the selective chemical stimulation of left ventricular receptors in the conscious dog. Twenty dogs were chronically instrumented to obtain measurements of arterial blood pressure, renal blood flow, and iliac blood flow before and after a bolus intracoronary injection of veratridine (0.4-1.0 micrograms/kg in 0.5-ml vol) with the heart paced. The responses to intracoronary veratridine were a significant reduction in arterial blood pressure averaging 25 mmHg accompanied by a simultaneous reduction in renal blood flow of 25%. Renal resistance did not change throughout the course of the response analyzed (50 s). Iliac blood flow, however, increased, reaching a peak of 35% above control due to a 51% decrease in iliac resistance. After sinoaortic denervation, renal resistance still failed to show a decrease, although the recovery of arterial blood pressure and iliac resistance was prolonged. After a mild hypotensive hemorrhage (20 ml/kg), a greater decrease in iliac resistance occurred with intracoronary veratridine injections, but renal resistance still did not change. The reduction in iliac resistance with intracoronary veratridine was significantly attenuated after phentolamine administration (2 mg/kg iv) but not after atropine alone (0.2 mg/kg iv). A significant cholinergic receptor component of iliac vasodilation was observed only after prior alpha-adrenergic-receptor blockade. The results of this study are consistent with the conclusion that in the conscious dog, left ventricular receptors exert a preferential neural control over skeletal muscle vascular resistance and do not influence renal vascular resistance.

Diverting renal and adrenal vein blood into liver and renal hypertension in dogs

1963 ◽  
Vol 205 (6) ◽  
pp. 1275-1278 ◽  
Author(s):  
W. G. Kubicek ◽  
A. P. Thal
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Vein ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Renal Vein ◽  
Adrenal Vein ◽  
Blood Pressure Elevation ◽  
Arterial Blood ◽  
Goldblatt Hypertension

The objectives of this investigation were: 1) To study the effect of diverting renal vein blood flow into the portal vein system upon renal function and hypertension produced by Goldblatt clamps. 2) To study the effects of passing the adrenal vein blood directly into the liver via the portal vein upon arterial blood pressure and upon Goldblatt hypertension. Renal vein blood was diverted into the portal vein by either a reverse Eck fistula or a direct renal to portal vein anastomosis. Clearance rates of p-aminohippurate and creatinine were used to measure renal blood flow and glomerular filtration rate. Goldblatt clamps on the renal arteries of four control dogs resulted in an average blood pressure elevation of 45/28 mm Hg. After a reverse Eck fistula in four dogs, average renal blood flow values indicated a fall of approximately 27% with no change in arterial blood pressure. Subsequent application of Goldblatt clamps resulted in an elevation in arterial blood pressure similar to the control animals. In two dogs, a direct renal to portal vein anastomosis yielded similar results. Diverting adrenal vein blood directly into the liver produced a small rise in the control arterial blood pressure and an apparent increase in the Goldblatt hypertension in two dogs.

Renovascular reactivity measured by near-infrared spectroscopy

2012 ◽  
Vol 113 (2) ◽  
pp. 307-314 ◽  
Author(s):  
Christopher J. Rhee ◽  
Kathleen K. Kibler ◽  
R. Blaine Easley ◽  
Dean B. Andropoulos ◽  
Marek Czosnyka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Infrared Spectroscopy ◽  
Hemorrhagic Shock ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Laser Doppler ◽  
Arterial Blood

Hypotension and shock are risk factors for death, renal insufficiency, and stroke in preterm neonates. Goal-directed neonatal hemodynamic management lacks end-organ monitoring strategies to assess the adequacy of perfusion. Our aim is to develop a clinically viable, continuous metric of renovascular reactivity to gauge renal perfusion during shock. We present the renovascular reactivity index (RVx), which quantifies passivity of renal blood volume to spontaneous changes in arterial blood pressure. We tested the ability of the RVx to detect reductions in renal blood flow. Hemorrhagic shock was induced in 10 piglets. The RVx was monitored as a correlation between slow waves of arterial blood pressure and relative total hemoglobin (rTHb) obtained with reflectance near-infrared spectroscopy (NIRS) over the kidney. The RVx was compared with laser-Doppler measurements of red blood cell flux, and renal laser-Doppler measurements were compared with cerebral laser-Doppler measurements. Renal blood flow decreased to 75%, 50%, and 25% of baseline at perfusion pressures of 60, 45, and 40 mmHg, respectively, whereas in the brain these decrements occurred at pressures of 30, 25, and 15 mmHg, respectively. The RVx compared favorably to the renal laser-Doppler data. Areas under the receiver operator characteristic curves using renal blood flow thresholds of 50% and 25% of baseline were 0.85 (95% CI, 0.83–0.87) and 0.90 (95% CI, 0.88–0.92). Renovascular autoregulation can be monitored and is impaired in advance of cerebrovascular autoregulation during hemorrhagic shock.

Effects of endothelin on renal function in dogs and rats

1990 ◽  
Vol 258 (4) ◽  
pp. F775-F780 ◽  
Author(s):  
R. O. Banks
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Function ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Left Renal Artery ◽  
Ang Ii ◽  
Arterial Blood ◽  
Entire Experiment

Endothelin was infused for 20 min into the left renal artery of pentobarbital-anesthetized dogs at 1 (n = 6) and 10 (n = 5) ng.min-1.kg-1. Renal blood flow (flow probe) increased 6 +/- 2 (SE) and 29 +/- 2% during the first 5 min of endothelin infusion and then slowly decreased to 86 +/- 3 and 29 +/- 2% of control at 20 min, respectively; the low renal blood flow persisted for at least 30 min after endothelin infusion, and there were no systemic effects of the peptide at either dose. These effects of endothelin on renal function were not altered by the angiotensin (ANG) II receptor antagonist, [Sar1,Thr8]ANG II. In the rat, endothelin was infused intravenously into three groups of pentobarbital-anesthetized females for 30 min at 0.1 microgram.min-1.kg-1; five had endothelin only, six had either endothelin + [Sar1,Thr8]ANG II (n = 4, 1.0 micrograms.min-1.kg-1) or endothelin + saralasin (n = 2, 1 and 2 micrograms.kg-1.min-1), and five had endothelin + captopril (5 mg.h-1.kg-1). The inhibitors were infused throughout the entire experiment. During infusion of endothelin alone mean arterial blood pressure increased from 106 +/- 2 to 136 +/- 4 mmHg and the glomerular filtration rate decreased from 2.7 +/- 0.2 to 0.7 +/- 0.3 ml/min. Captopril attenuated the endothelin-induced changes in renal function but not the increase in mean arterial blood pressure, whereas the competitive ANG II receptor antagonists had no effect on either the systemic or renal actions of the peptide. These data demonstrate that endothelin is a potent renal vasoconstrictor with transient vasodilator effects and that the inhibition of kinin degradation may attenuate the renal actions of the peptide.

Cardiovascular responses to V1-vasopressinergic antagonism in conscious versus anesthetized rats

1988 ◽  
Vol 66 (11) ◽  
pp. 1437-1441 ◽  
Author(s):  
Barbara L. Brizzee ◽  
Benjimen R. Walker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Arginine Vasopressin ◽  
Surgical Stress ◽  
Arterial Blood ◽  
Anesthetized Rats

Experiments were performed to compare the possible effect of endogenous arginine vasopressin on renal hemodynamics between anesthetized, surgically stressed rats and conscious rats. Animals were instrumented with arterial and venous catheters as well as with a pulsed Doppler flow probe on the left renal artery. The rats were studied under the following conditions: (1) conscious and unrestrained; (2) anesthetized only; (3) anesthetized with minor surgical stress; and (4) anesthetized with major surgical stress. Two anesthetic agents were also compared, a mixture of ketamine (110 mg/kg i.m.) and acepromazine (1 mg/kg i.m.), and sodium pentobarbital (50 mg/kg i.p.). Baseline mean arterial blood pressure was significantly higher in pentobarbital-anesthetized rats following surgical stress compared with conscious animals, but blood pressure was not affected by ketamine–acepromazine anesthesia. After baseline measurements of blood pressure, heart rate, and renal blood flow, a specific V1-vasopressinergic antagonist (d(CH2)5Tyr(Me) arginine vasopressin, 10 mg/kg i.v.) was administered to each group. Mean arterial blood pressure, heart rate, and renal blood flow were monitored for an additional 15 min. Mean arterial blood pressure and renal blood flow decreased after V1 antagonism in ketamine–acepromazine-anesthetized rats with major surgical stress, but were not affected in pentobarbital-anesthetized animals. Heart rate and renal vascular resistance were not affected following V1 blockade with either anesthetic agent. These data suggest that arginine vasopressin plays a role in maintaining blood pressure and renal perfusion in ketamine–acepromazine-anesthetized rats following surgical stress, but does not have a significant effect on renal hemodynamics under pentobarbital anesthesia.

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