Effects of Intracisternal and Intravenous α-Methyldopa and Clonidine on Haemodynamics and Baroreceptor-Heart Rate Reflex Properties in Conscious Rabbits

1983 ◽  
Vol 5 (5) ◽  
pp. 760-767 ◽  
Author(s):  
E. Badoer ◽  
G. A. Head ◽  
P. I. Korner
Keyword(s):  
Heart Rate ◽  
Conscious Rabbits

Does nitric oxide contribute to the basal vasodilation of pregnancy in conscious rabbits?

2001 ◽  
Vol 281 (5) ◽  
pp. R1624-R1632 ◽  
Author(s):  
Virginia L. Brooks ◽  
Kathy A. Clow ◽  
Lisa S. Welch ◽  
George D. Giraud
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Mesenteric Artery ◽  
Vascular Tone ◽  
Ascending Aorta ◽  
No Production ◽  
Vascular Conductance ◽  
Vascular Beds ◽  
Conscious Rabbits

Pregnancy produces marked systemic vasodilation, but the mechanism is unknown. Experiments were performed in conscious rabbits to test the hypotheses that increased nitric oxide (NO) production contributes to the increased vascular conductance, but that the contribution varies among vascular beds. Rabbits were instrumented with aortic and vena caval catheters and ultrasonic flow probes implanted around the ascending aorta, superior mesenteric artery, terminal aorta, and/or a femoral artery. Hemodynamic responses to intravenous injection of N ω-nitro-l-arginine (l-NA; 20 mg/kg or increasing doses of 2, 5, 10, 15, and 20 mg/kg) were determined in rabbits first before pregnancy (NP) and then at the end of gestation (P). l-NA produced similar increases in arterial pressure between groups, but the following responses were larger ( P < 0.05) when the rabbits were pregnant: 1) decreases in total peripheral conductance [−3.7 ± 0.3 (NP), −5.0 ± 0.5 (P) ml · min−1 · mmHg−1], 2) decreases in mesenteric conductance [−0.47 ± 0.05 (NP), −0.63 ± 0.07 (P) ml · min−1 · mmHg−1], 3) decreases in terminal aortic conductance [−0.43 ± 0.05 (NP), −0.95 ± 0.19 ml · min−1 · mmHg−1 (P)], and 4) decreases in heart rate [−41 ± 4 (NP), −62 ± 5 beats/min (P)]. Nevertheless, total peripheral and terminal aortic conductances remained elevated in the pregnant rabbits ( P < 0.05) after l-NA. Furthermore, decreases in cardiac output and femoral conductance were not different between the reproductive states. We conclude that the contribution of NO to vascular tone increases during pregnancy, but only in some vascular beds. Moreover, the data support a role for NO in the pregnancy-induced increase in basal heart rate. Finally, unknown factors in addition to NO must also underlie the basal vasodilation observed during pregnancy.

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.

Central nitric oxide attenuates the baroreceptor reflex in conscious rabbits

1998 ◽  
Vol 274 (4) ◽  
pp. R1142-R1149 ◽  
Author(s):  
Kiyoshi Matsumura ◽  
Isao Abe ◽  
Takuya Tsuchihashi ◽  
Masatoshi Fujishima
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Methyl Ester ◽  
Pressor Response ◽  
Baroreceptor Reflex ◽  
Plasma Catecholamine ◽  
No Donor ◽  
Baroreflex Control ◽  
Intracerebroventricular Infusion ◽  
Conscious Rabbits

We examined the role of central nitric oxide (NO) in the baroreceptor reflex in conscious rabbits. Intracerebroventricular infusion of 20 μmol of N ω-nitro-l-arginine methyl ester (l-NAME) to block central NO resulted in increases in arterial pressure, renal sympathetic nerve activity (RSNA), and plasma catecholamine levels, and the pressor response was suppressed by pretreatment with pentolinium (5 mg/kg iv). On the other hand, a subpressor dose of intracerebroventricular l-NAME (10 μmol/h) caused significant increases in baroreflex sensitivities assessed by RSNA and heart rate compared with vehicle infusion [maximum gain: −18.2 ± 0.9 vs. −9.6 ± 0.9%/mmHg ( P < 0.001) and −14.3 ± 2.3 vs. −5.7 ± 0.4 beats ⋅ min−1 ⋅ mmHg−1( P < 0.05), respectively]. Conversely, an intracerebroventricular infusion of Et2N[N(O)NO]Na, an NO donor (1 μmol/h) significantly attenuated the baroreflex sensitivities. However, intracerebroventricular infusion of N ω-nitro-d-arginine methyl ester (10 μmol/h), an enantiomer ofl-NAME, failed to alter the baroreflex sensitivities. These results suggest that 1) the pressor response induced by inhibition of central NO synthesis is mainly mediated by the enhanced sympathetic outflow and 2) central NO attenuates the baroreflex control of RSNA and heart rate in conscious rabbits.

Comparison of the baroreceptor–heart rate reflex effects of moxonidine, rilmenidine and clonidine in conscious rabbits

1998 ◽  
Vol 72 (2-3) ◽  
pp. 195-204 ◽  
Author(s):  
Shirley J. Godwin ◽  
Connie F. Tortelli ◽  
Monique L. Parkin ◽  
Geoffrey A. Head
Keyword(s):  
Heart Rate ◽  
Conscious Rabbits

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.

Hemodynamic and hormonal responses to hemorrhage in conscious rabbits at mid- and late gestation

1998 ◽  
Vol 275 (4) ◽  
pp. R1082-R1090 ◽  
Author(s):  
Virginia L. Brooks ◽  
Rebecca R. Quesnell ◽  
Colleen M. Kane ◽  
Lanny C. Keil
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Plasma Renin ◽  
Late Gestation ◽  
Ang Ii ◽  
Pressure Regulation ◽  
Hormonal Responses ◽  
Conscious Rabbits ◽  
The Relationship ◽  
Arterial Pressure Regulation

This study tests the hypothesis that conscious rabbits late in pregnancy (P), but not at midgestation (MP), are less able to maintain arterial pressure during hemorrhage. Blood volume (BV) was elevated ( P < 0.05) by an average of 13 ± 4 (MP) and 35 ± 3% (P). Rabbits were bled in both the nonpregnant (NP) and P state at 2% of the initial BV per minute. The hemorrhage was stopped after arterial pressure decreased. In NP rabbits, arterial pressure was well maintained near control pressures of 70 ± 2 mmHg until 38 ± 2% of the initial BV was removed and then rapidly fell to reach a nadir at 35 ± 2 mmHg. In contrast, in P rabbits, basal arterial pressure was lower (61 ± 2 mmHg; P < 0.05) and gradually decreased to below control after <25% of the initial BV was removed. Moreover, the rapid hypotensive phase was triggered with a lower percent BV removal (33 ± 2%; P < 0.05). Basal heart rate was higher during P (149 ± 5 vs. 189 ± 9 beats/min; P < 0.05), and reflex increases were delayed. The slope of the relationship between arterial pressure and vasopressin was not modified during P, although the line was shifted to a lower pressure ( P < 0.05). Larger increases in plasma renin activity and ANG II concentration were produced during hemorrhage in P rabbits. In contrast, no differences in the changes in arterial pressure, heart rate, and vasopressin were found between NP and MP rabbits during hemorrhage, although increases in renin and ANG II were greater at MP ( P < 0.05). In summary, although P conscious rabbits are less able to maintain blood pressure during hemorrhage, this change is not evident at MP. These data suggest that the factors that mediate the P-induced alterations in arterial pressure regulation are not operative until late in gestation.

Lesions of A1 noradrenergic cells affect AVP release and heart rate during hemorrhage

1987 ◽  
Vol 253 (5) ◽  
pp. H1012-H1017 ◽  
Author(s):  
G. A. Head ◽  
A. W. Quail ◽  
R. L. Woods
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Volume ◽  
Ventrolateral Medulla ◽  
Sham Operation ◽  
Noradrenergic Neurons ◽  
Reflex Tachycardia ◽  
Conscious Rabbits ◽  
Plasma Arginine

The role of A1 noradrenergic cells of the ventrolateral medulla in the changes in mean arterial pressure (MAP), heart rate (HR), and plasma arginine vasopressin (AVP) after slow continuous hemorrhage (2% blood vol/min up to 35%) was examined by comparing responses in conscious rabbits before and 3 wk after a sham operation or A1 lesions. In the control experiments, MAP fell minimally up to the withdrawal of 20% of blood volume after which it fell abruptly to 20-30 mmHg below control by the 35% level. Plasma AVP increased nonlinearly during progressive hemorrhage with significant increases occurring only after 25% of blood volume was removed. In contrast, HR increased linearly after the onset of bleeding. After A1 lesions, which destroyed 84% (range 80-94%) of the noradrenergic cells, the amount of AVP released and the tachycardia during hemorrhage were reduced by 83 and 61%, respectively (P less than 0.005), but the fall in MAP was minimally affected. Basal values of MAP, HR, or plasma AVP were not affected by the lesions. These results suggest that during hemorrhage in conscious rabbits A1 noradrenergic neurons are important for the secretion of AVP and the reflex tachycardia but play little role in the maintenance of blood pressure.

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