EFFECTS OF ENDOTHELIN-1 ON ARTERIAL PRESSURE: A COMPARISON OF INTRAVENOUS AND INTRA-ARTERIAL ADMINISTRATION IN CONSCIOUS RABBITS

1994 ◽  
Vol 21 (4) ◽  
pp. 323-327
Author(s):  
P. Roberts-Thomson ◽  
R. J. McRitchie ◽  
M. D. Cain ◽  
J. P. Chalmers
Keyword(s):  
Arterial Pressure ◽  
Endothelin 1 ◽  
Conscious Rabbits

ROK contribution to endothelin-mediated contraction in aorta and mesenteric arteries following intermittent hypoxia/hypercapnia in rats

2007 ◽  
Vol 293 (5) ◽  
pp. H2911-H2918 ◽  
Author(s):  
Kyan J. Allahdadi ◽  
Benjimen R. Walker ◽  
Nancy L. Kanagy
Keyword(s):  
Arterial Pressure ◽  
Light Chain ◽  
Myosin Light Chain Kinase ◽  
Intermittent Hypoxia ◽  
Myosin Light Chain ◽  
Mesenteric Arteries ◽  
Endothelin 1 ◽  
Second Messenger Systems ◽  
Intracellular Ca ◽  
Inner Diameter

We reported previously that intermittent hypoxia with CO2 to maintain eucapnia (IH-C) elevates plasma endothelin-1 (ET-1) and arterial pressure. In small mesenteric arteries (sMA; inner diameter = 150 μm), IH-C augments ET-1 constrictor sensitivity but diminishes ET-1-induced increases in intracellular Ca2+ concentration, suggesting IH-C exposure increases both ET-1 levels and ET-1-stimulated Ca2+ sensitization. Because Rho-associated kinase (ROK) can mediate Ca2+ sensitization, we hypothesized that augmented vasoconstrictor sensitivity to ET-1 in arteries from IH-C-exposed rats is dependent on ROK activation. In thoracic aortic rings, ET-1 contraction was not different between groups, but ROK inhibition (Y-27632, 3 and 10 μM) attenuated ET-1 contraction more in IH-C than in sham arteries (50 ± 11 and 78 ± 7% vs. 41 ± 12 and 48 ± 9% inhibition, respectively). Therefore, ROK appears to contribute more to ET-1 contraction in IH-C than in sham aorta. In sMA, ROK inhibitors did not affect ET-1-mediated constriction in sham arteries and only modestly inhibited it in IH-C arteries. In ionomycin-permeabilized sMA with intracellular Ca2+ concentration held at basal levels, Y-27632 did not affect ET-1-mediated constriction in either IH-C or sham sMA and ET-1 did not stimulate ROK translocation. In contrast, inhibition of myosin light-chain kinase (ML-9, 100 μM) prevented ET-1-mediated constriction in sMA from both groups. Therefore, IH-C exposure increases ET-1 vasoconstrictor sensitivity in sMA but not in aorta. Furthermore, ET-1 constriction is myosin light-chain kinase dependent and mediated by Ca2+ sensitization that is independent of ROK activation in sMA but not aorta. Thus ET-1-mediated signaling in aorta and sMA is altered by IH-C but is dependent on different second messenger systems in small vs. large arteries.

Contribution of renal nerves to renal blood flow variability during hemorrhage

1998 ◽  
Vol 274 (5) ◽  
pp. R1283-R1294 ◽  
Author(s):  
Simon C. Malpas ◽  
Roger G. Evans ◽  
Geoff A. Head ◽  
Elena V. Lukoshkova
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Spectral Power ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Similar Frequency ◽  
Blood Withdrawal ◽  
Conscious Rabbits ◽  
Renal Sympathetic

We have examined the role of the renal sympathetic nerves in the renal blood flow (RBF) response to hemorrhage in seven conscious rabbits. Hemorrhage was produced by blood withdrawal at 1.35 ml ⋅ min−1 ⋅ kg−1for 20 min while RBF and renal sympathetic nerve activity (RSNA) were simultaneously measured. Hemorrhage was associated with a gradual increase in RSNA and decrease in RBF from the 4th min. In seven denervated animals, the resting RBF before hemorrhage was significantly greater (48 ± 1 vs. 31 ± 1 ml/min intact), and the decrease in RBF did not occur until arterial pressure also began to fall (8th min); however, the overall percentage change in RBF by 20 min of blood withdrawal was similar. Spectral analysis was used to identify the nature of the oscillations in each variable. Before hemorrhage, a rhythm at ∼0.3 Hz was observed in RSNA, although not in RBF, whose spectrogram was composed mostly of lower-frequency (<0.25 Hz) components. The denervated group of rabbits had similar frequency spectrums for RBF before hemorrhage. RSNA played a role in dampening the effect of oscillations in arterial pressure on RBF as the transfer gain between mean arterial pressure (MAP) and RBF for frequencies >0.25 Hz was significantly less in intact than denervated rabbits (0.83 ± 0.12 vs. 1.19 ± 0.10 ml ⋅ min−1 ⋅ mmHg−1). Furthermore, the coherence between MAP and RBF was also significantly higher in denervated rabbits, suggesting tighter coupling between the two variables in the absence of RSNA. Before the onset of significant decreases in arterial pressure (up to 10 min), there was an increase in the strength of oscillations centered around 0.3 Hz in RSNA. These were accompanied by increases in the spectral power of RBF at the same frequency. As arterial pressure fell in both groups of animals, the dominant rhythm to emerge in RBF was centered between 0.15 and 0.20 Hz and was present in intact and denervated rabbits. It is speculated that this is myogenic in origin. We conclude that RSNA can induce oscillations in RBF at 0.3 Hz, plays a significant role in altering the effect of oscillations in arterial pressure on RBF, and mediates a proportion of renal vasoconstriction during hemorrhage in conscious rabbits.

Cardiovascular and neurohormonal effects of intravenous adrenomedullin in conscious rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. R1289-R1293 ◽  
Author(s):  
M. Fukuhara ◽  
T. Tsuchihashi ◽  
I. Abe ◽  
M. Fujishima
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Conscious Rabbits ◽  
Renal Sympathetic

Adrenomedullin is a vasodilative peptide and shows slight homology with calcitonin gene-related peptide. In the present study, we investigated the effects of adrenomedullin on cardiovascular and neurohormonal responses in 13 conscious rabbits. The animals were chronically instrumented with bipolar electrodes on the left renal sympathetic nerve. Intravenous administration of human adrenomedullin (10, 100, 1,000, and 3,000 pmol/kg, n = 6) caused a dose-dependent reduction in mean arterial pressure (0 +/- 2, -1 +/- 2, -19 +/- 2, and -29 +/- 4 mmHg, respectively) concomitant with increases in heart rate, renal sympathetic nerve activity, plasma renin activity, and plasma norepinephrine. The significant reduction in mean arterial pressure induced by 1,000 pmol/kg of adrenomedullin occurred within 1 min after injection and lasted for 15 min (n = 7). In contrast, the significant increases in heart rate and renal sympathetic nerve activity lasted for more than 50 min. When mean arterial pressure was decreased by 15 mmHg by adrenomedullin, the increases in heart rate and renal sympathetic nerve activity were 53 +/- 8 beats/min and 78 +/- 13%, respectively, which were significantly smaller than those induced by intravenous injection of sodium nitroprusside (102 +/- 14 beats/min and 155 +/- 34%, respectively). These results suggest that intravenous adrenomedullin exerts a hypotensive action that is associated with the attenuated reflex-mediated sympathetic activation.

Regional conductance changes during hemorrhage in pregnant and nonpregnant conscious rabbits

1999 ◽  
Vol 277 (3) ◽  
pp. R675-R681 ◽  
Author(s):  
Virginia L. Brooks ◽  
Colleen M. Kane ◽  
Lisa S. Welch
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Late Gestation ◽  
Blood Pressure Fall ◽  
Conductance Changes ◽  
Conscious Rabbits ◽  
The Difference ◽  
Initial Blood ◽  
Pressure Fall

Late pregnant (P) conscious rabbits are less able to maintain arterial pressure during hemorrhage than nonpregnant (NP) animals. This study tested the hypothesis that the difference is due in part to less reflex vasoconstriction when the rabbits are P. Rabbits ( n = 14) were instrumented with arterial and venous catheters as well as ultrasonic flow probes around the superior mesenteric, renal, and/or terminal aortic arteries. Pregnancy increased ( P < 0.05) blood volume [235 ± 5 (P) vs. 171 ± 3 (NP) ml], terminal aortic conductance [1.88 ± 0.11 (P) vs. 0.98 ± 0.06 (NP) ml ⋅ min−1 ⋅ mmHg−1], mesenteric conductance [1.20 ± 0.19 (P) vs. 0.80 ± 0.05 (NP) ml ⋅ min−1 ⋅ mmHg−1], and heart rate [191 ± 4 (P) vs. 162 ± 3 (NP) beats/min] and decreased arterial pressure [59 ± 1 (P) vs. 67 ± 2 (NP) mmHg; P < 0.05]. Renal conductance was unaltered. The rabbits were bled in both the NP and P states at 2% of the initial blood volume per minute until arterial pressure fell below 45 mmHg. Arterial pressure fell with less blood loss in P rabbits [28 ± 2% (P) vs. 39 ± 2% (NP) of initial blood volume; P < 0.001]. Terminal aortic conductance decreased ( P < 0.001) before the pressure fall in both groups, but the response was reduced in P rabbits. Mesenteric and renal conductances did not change in either group before the blood pressure fall. During the pressure fall, terminal aortic conductance increased ( P < 0.05) only in NP rabbits. Mesenteric conductance increased in both groups. In summary, rabbits in late gestation are less able to maintain arterial pressure during hemorrhage, at least in part because of reduced vasoconstriction in tissues perfused by the terminal aorta.

Cutaneous vasoconstriction in conscious rabbits during alerting responses detected by hippocampal theta-rhythm

1997 ◽  
Vol 272 (1) ◽  
pp. R208-R216 ◽  
Author(s):  
Y. H. Yu ◽  
W. W. Blessing
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Theta Rhythm ◽  
Renal Flow ◽  
Conscious Rabbits ◽  
Hippocampal Theta ◽  
Electroencephalogram Eeg ◽  
Cutaneous Vasoconstriction

We determined whether alerting stimuli cause cutaneous vasoconstriction in conscious rabbits. We compared ear blood flow with renal, mesenteric, and femoral flows at rest and in response to nonnoxious alerting stimuli, which induced theta-rhythm (4-9 Hz) in the simultaneously recorded hippocampal electroencephalogram (EEG). theta-Inducing stimuli (e.g., whistles and fur touches) reduced ear flow by 95 +/- 6%, commencing 1-2 s after the EEG change and lasting 45 s. Renal flow did not significantly change with alerting stimuli, mesenteric and femoral flows slightly decreased, arterial pressure transiently rose (+10 +/- 3 mmHg), and heart rate fell (+43 +/- 9 beats/min). At rest, the coefficient of variation for ear flow (62 +/- 6%) was greater than for other flows (P < 0.01). Phentolamine (1 mg/kg iv) reduced this coefficient to 29 +/- 4% (P < 0.01). Our study demonstrates that alerting responses in conscious rabbits are associated with selective cutaneous vasoconstriction, without increase in flow to skeletal muscle.

Interaction of acetylcholine and endothelin-1 in the modulation of pulmonary arterial pressure

2000 ◽  
Vol 28 (12) ◽  
pp. 3869-3875 ◽  
Author(s):  
Joachim Schmeck ◽  
Christoph Konrad ◽  
Susanne Schöffel ◽  
Martina Wendel-Wellner ◽  
H. Gluth ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Endothelin 1 ◽  
Pulmonary Arterial

Effects of a new dihydropyridine derivative, S12968 (pranedipine), and its stereoisomer, S12967, on renal effects of endothelin-1

1994 ◽  
Vol 72 (11) ◽  
pp. 1294-1298 ◽  
Author(s):  
Immaculada Montañés ◽  
Olga Flores ◽  
Nélida Eleno ◽  
José M. López-Novoa
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Fold Increase ◽  
Urine Flow ◽  
Renal Vascular Resistance ◽  
Potassium Excretion ◽  
Endothelin 1 ◽  
Dihydropyridine Derivative ◽  
Renal Vascular

The purpose of the present study was to assess in rats the prevention by two enantiomers of a new dihydropyridine derivative (pranedipine) (called S12967 for the dextrogyre(+) and S12968 for the levogyre (−) molecules) of the renal and cardiovascular effects induced by endothelin-1. The injection of endothelin-1 (1 nmol/kg body weight) induced a sharp and transient decrease in urine flow, sodium and potassium excretion, glomerular filtration rate, renal plasma flow, and renal blood flow, a significant increase in renal vascular resistance, and a small but significant increase in arterial pressure. Treatment with S12968 alone (0.3 mg/kg) induced a 2.5-fold increase in urine flow and potassium excretion and a 4.5-fold increase in sodium excretion. Pretreatment with S12968 completely blocked the endothelin-1 induced increase in arterial pressure, did not affect the acute effect of endothelin-1 on urine flow, sodium and potassium excretion, filtration rate, and renal blood flow, but blunted the effect on renal vascular resistance. Administration of S12967 alone (1 mg/kg) did not induce changes in either renal function or arterial pressure. In S12967-treated animals, endothelin-1 also induced a transient increase in arterial pressure and renal vascular resistance but failed to change renal function in a significant manner. In summary, the above reported experiments show that at the higher, nonhypotensive doses, the levogyre enantiomer (S12968) of a new dihydropyridine derivative (pranedipine) completely prevented the hypertensive effect of endothelin 1, and partially prevented the effect of endothelin-1 on renal vascular resistance. The dextrogyre enantiomer (S12967) had almost no effect on either mean arterial pressure or renal vascular resistance but completely blocked the endothelin-1-induced decrease in urine flow and urinary sodium excretion.Key words: calcium antagonists, endothelin, dihydropyridines, kidney, renal function (rat).

scholarly journals Central Human Cocaine- and Amphetamine-Regulated Transcript Peptide 55–102 Increases Arterial Pressure in Conscious Rabbits

Hypertension ◽  
2001 ◽  
Vol 38 (5) ◽  
pp. 1096-1100 ◽  
Author(s):  
Kiyoshi Matsumura ◽  
Takuya Tsuchihashi ◽  
Isao Abe
Keyword(s):  
Arterial Pressure ◽  
Conscious Rabbits

The Effects of Meclofenamate, Captopril and Phentolamine on Organ Blood Flow in the Conscious Rabbit

1981 ◽  
Vol 61 (1) ◽  
pp. 97-105 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Hepatic Artery ◽  
Peripheral Resistance ◽  
Prostaglandin Synthesis ◽  
Organ Blood Flow ◽  
Inhibit Prostaglandin Synthesis ◽  
Conscious Rabbits ◽  
Artery Flow ◽  
Intravenous Sodium

1. Systemic and regional vascular changes were measured in conscious rabbits after intravenous sodium meclofenamate, captopril and phentolamine. These drugs were used respectively to inhibit prostaglandin synthesis and angiotensin-converting enzyme, and to block α-adrenoceptors. 2. Meclofenamate reduced renal and adrenal blood flow by 11 and 28% respectively, and doubled hepatic artery flow. The effect on renal and adrenal flow persisted in the presence of phentolamine. 3. Captopril decreased estimated peripheral resistance and increased cardiac output without changing arterial pressure. Kidney and adrenal flow increased by 70 and 21% respectively. 4. Phentolamine reduced arterial pressure and doubled flow to skeletal muscle and increased hepatic artery flow to the liver. 5. Splenic blood flow was unaffected by meclofenamate, captopril or phentolamine alone. Meclofenamate given after captopril caused a halving of splenic flow and a rise in arterial pressure; these effects were prevented by phentolamine. 6. The results point to a continuing effect of prostaglandin synthesis in maintaining blood flow to the kidney and adrenal gland independent of α-adrenoceptor activation in resting conscious rabbits. An important modulating effect of prostaglandins on sympathetic vascular tone in the spleen is suggested.

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