Analysis of the afferent limb of the vesicovascular reflex using neurotoxins, resiniferatoxin and capsaicin

2001 ◽  
Vol 281 (4) ◽  
pp. R1302-R1310 ◽  
Author(s):  
Yao-Chi Chuang ◽  
Matthew O. Fraser ◽  
Yongbei Yu ◽  
Jonathan M. Beckel ◽  
Satoshi Seki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Urinary Bladder ◽  
Arterial Blood Pressure ◽  
Pressor Response ◽  
Female Rats ◽  
Luminal Surface ◽  
Intravesical Administration ◽  
Afferent Limb ◽  
Arterial Blood ◽  
C Fiber

The afferent limb of the vesicovascular reflex (VV-R) evoked by distension or contraction of the urinary bladder (UB) was studied in urethane-anesthetized female rats by examining the changes in VV-R after administration of C-fiber afferent neurotoxins [capsaicin and resiniferatoxin (RTX)]. Systemic arterial blood pressure increased parallel (5.1 to 53.7 mmHg) with graded increases in UB pressure (20 to 80 cmH2O) or during UB contractions. The arterial pressor response to UB distension was significantly reduced (60–85%) by acute or chronic (4 days earlier) intravesical administration of RTX (100–1,000 nM) or by capsaicin (125 mg/kg sc) pretreatment (4 days earlier). Chronic neurotoxin treatments also increased the volume threshold (>100%) for eliciting micturition in anesthetized rats but did not change voiding pressure. Acute RTX treatment (10–50 nM) did not alter the arterial pressor response during reflex UB contractions, whereas higher concentrations of RTX (100–1,000 nM) blocked reflex bladder contractions. It is concluded that VV-R is triggered primarily by distension- and contraction-sensitive C-fiber afferents located, respectively, near the luminal surface and deeper in the muscle layers of the bladder.

Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Response To Exercise ◽  
Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

Effect of norepinephrine on plasma free fatty acids in dogs treated with reserpine

1963 ◽  
Vol 205 (1) ◽  
pp. 57-59 ◽  
Author(s):  
Francois M. Abboud ◽  
Michael G. Wendling ◽  
John W. Eckstein
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Arterial Blood Pressure ◽  
Pressor Response ◽  
Maximal Increase ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Plasma Ffa

Some adrenergic blocking drugs reduce the mobilization of free fatty acids (FFA) in response to administration of catecholamines. The present experiments were done to see if potentiation of the pressor effect of norepinephrine by reserpine is accompanied by a greater increase in plasma FFA. Norepinephrine was infused intravenously into 16 anesthetized dogs. Eight of them had been treated with reserpine, 0.25 mg/kg daily, intraperitoneally for 2 days; the others were not treated. Arterial blood samples were drawn before, during, and after norepinephrine for determination of plasma FFA concentrations. Systemic arterial blood pressure was measured continuously. In the treated animals the maximal increase in arterial blood pressure as well as the progressive increments in FFA concentration were greater than in the untreated dogs. The experiments indicate that potentiation of the pressor response to norepinephrine after reserpine is accompanied by a greater FFA response.

Cardiovascular control during voluntary static exercise in humans with tetraplegia

2004 ◽  
Vol 97 (6) ◽  
pp. 2077-2082 ◽  
Author(s):  
Makoto Takahashi ◽  
Akihiro Sakaguchi ◽  
Kanji Matsukawa ◽  
Hidehiko Komine ◽  
Kotaro Kawaguchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cervical Spinal Cord ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Voluntary Contraction ◽  
Static Exercise ◽  
Arm Exercise ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C6-C7). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.

Effects of vasopressin on arterial blood pressure and cardiac output in male and female rats

1991 ◽  
Vol 261 (5) ◽  
pp. R1118-R1125 ◽  
Author(s):  
K. Toba ◽  
J. T. Crofton ◽  
M. Inoue ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Arterial Blood ◽  
Male And Female Rats ◽  
Cycle Dependent

This study was performed to investigate further the mechanisms underlying the sexual dimorphism of the pressor responses to vasopressin. We have confirmed our earlier findings that the pressor response to graded infusions of vasopressin in conscious unrestrained male rats is similar to that in estrous females and greater than in diestrus, proestrus, and metestrus. This difference was due primarily to greater increases in total peripheral resistance (TPR) in males and estrous females, since there were no sex- or cycle-related differences in the vasopressin-induced reductions in cardiac output. Gonadectomy was without effect in males but, in females, increased blood pressure responses to vasopressin to levels found in males. Chronic treatment of ovariectomized rats with estradiol reduced pressor responsiveness to vasopressin; treatment with progesterone was without effect. These differences were also due to differences in TPR. It is concluded that the sex- and cycle-dependent differences in vasopressin-induced increases in blood pressure are due largely to attenuation of increases in TPR by estrogen.

Evaluation of Arterial Blood Pressure and Renal Sodium Handling in a Model of Female Rats in Persistent Estrus

2010 ◽  
Vol 32 (6) ◽  
pp. 385-389 ◽  
Author(s):  
José Antonio Rocha Gontijo ◽  
Daniela C. Gui ◽  
Patrícia Aline Boer ◽  
Alesse Ribeiro Dos Santos ◽  
Celso Pires Ferreira-filho ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Female Rats ◽  
Arterial Blood ◽  
Persistent Estrus ◽  
Renal Sodium Handling ◽  
Sodium Handling

Comparative study of pressor and heart rate responses to angiotensin II and noradrenaline in pregnant and non-pregnant women

1992 ◽  
Vol 82 (2) ◽  
pp. 157-162 ◽  
Author(s):  
Margaret Ramsay ◽  
Fiona Broughton Pipkin ◽  
Peter Rubin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Pregnant Women ◽  
Arterial Blood Pressure ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Arterial Blood ◽  
Diastolic Arterial Blood Pressure ◽  
In Pregnancy

1. Twenty-eight healthy non-pregnant women and 28 women in the first or second trimester of pregnancy were studied. They were given an incremental intravenous infusion of either noradrenaline or angiotensin II. Pressor and heart rate responses were documented. 2. Dose-pressor response curves were constructed for the two agents in pregnant and non-pregnant women (n=14 in each group). The regression parameters of slope and intercept were calculated, and were used to derive the variables of dose required to elicit a 10 mmHg rise in systolic or diastolic blood pressure. 3. The pressor response to angiotensin II was diminished in pregnancy, with approximately twice the dose being required to raise the systolic or diastolic arterial blood pressure as in non-pregnant subjects. 4. The systolic pressor response to noradrenaline was slightly diminished in pregnancy, but the diastolic pressor response was unchanged. There were no significant differences between the doses of noradrenaline required to elicit a 10 mmHg rise in systolic or diastolic arterial blood pressure in pregnant or non-pregnant subjects. 5. There was a diminution in the bradycardia evoked in response to both hormones in pregnancy. 6. We conclude that the well-documented pressor insensitivity to angiotensin II during pregnancy is a specific phenomenon, not a manifestation of a generalized reduction in vascular reactivity.

Plasma Noradrenaline and the Pressor Action of Exogenous Noradrenaline in Normotensive Subjects and Patients with Essential Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 61s-63s ◽  
Author(s):  
T. Philipp ◽  
A. Distler ◽  
U. Cordes ◽  
H. P. Wolff
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Arterial Blood Pressure ◽  
Inverse Relationship ◽  
Pressor Response ◽  
Blood Pressure Level ◽  
Plasma Noradrenaline ◽  
Arterial Blood ◽  
Adrenergic Activity ◽  
Normotensive Subjects

1. An inverse relationship was found between plasma noradrenaline and reactivity to exogenous noradrenaline in normotensive subjects. 2. The relationship between plasma noradrenaline and reactivity was disturbed in age-matched patients with essential hypertension. 3. A multiple-regression analysis showed a highly significant correlation between adrenergic activity and reactivity to noradrenaline and the mean arterial blood pressure level (r = 0·91). The results suggest that adrenergic activity and pressor response to noradrenaline combined are important determinants of arterial blood pressure. 4. An inverse relationship could also be demonstrated between plasma renin activity and reactivity to exogenous angiotensin II. No difference was observed between normotensive and hypertensive subjects.

Effects of the angiotensin II receptor antagonist Losartan (DuP 753/MK 954) on arterial blood pressure, heart rate, plasma concentrations of angiotensin II and renin and the pressor response to infused angiotensin II in the salt-deplete dog

1992 ◽  
Vol 83 (5) ◽  
pp. 549-556 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Plasma Angiotensin

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1–3 μmin−1 kg−1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min−1kg−1), and a dose of 10 μgmin−1 kg−1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 μmin−1 kg−1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 ± 11.2 to 95.0 ± 12.8 mmHg) and a rise in heart rate (from 84.6 ± 15.1 to 103 ± 15.2 beats/min). Baseline plasma angiotensin II (42.5 ± 11.8 pg/ml) and renin (64.5 ± 92.7 μ-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 ± 11.6 mmHg) was reduced at 15 min (11.8 ± 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 ± 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ngmin−1kg−1, +19.9 ± 8 mmHg; 2000ngmin−1 kg−1, +52.8 ± 13.9 mmHg) with a fall in heart rate (1000 ng min−1 kg−1, −27.9 ± 11.5 beats/min; 2000 ng min−1 kg−1, −31.2 ± 17.3 beats/min). During Losartan infusion the 1000 but not the 2000 ng min−1 kg−1 noradrenaline infusion caused a greater rise in mean arterial blood pressure and a greater fall in heart rate. The fall in heart rate tended to decrease with continued infusion of Losartan. Plasma catecholamine concentrations were unaffected by Losartan. In a further study, higher doses of Losartan (100, 300 and 1000 μg min−1 kg−1; 30 min) produced greater falls in mean arterial blood pressure also with a rise in heart rate and complete blockade of the pressor effect of infused angiotensin II. Some animals became disturbed at the highest dose. 3. Losartan produces rapid dose-related falls in blood pressure and a rise in heart rate and renin release with elevation of plasma angiotensin II. Pressor responses to angiotensin II are reduced at intermediate doses and are eliminated at high doses. Losartan does not appear to inhibit angiotensin II clearance from the plasma and may in some way increase it.

scholarly journals Roles of baroreflex and vestibulosympathetic reflex in controlling arterial blood pressure during gravitational stress in conscious rats

2004 ◽  
Vol 286 (1) ◽  
pp. R25-R30 ◽  
Author(s):  
Taro Miyahara Gotoh ◽  
Nobuhiro Fujiki ◽  
Tomoko Matsuda ◽  
Shuang Gao ◽  
Hironobu Morita
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Pressor Response ◽  
Circulatory System ◽  
Intact Group ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Gravitational Stress ◽  
Vestibulosympathetic Reflex ◽  
Blood Redistribution

Gravity acts on the circulatory system to decrease arterial blood pressure (AP) by causing blood redistribution and reduced venous return. To evaluate roles of the baroreflex and vestibulosympathetic reflex (VSR) in maintaining AP during gravitational stress, we measured AP, heart rate (HR), and renal sympathetic nerve activity (RSNA) in four groups of conscious rats, which were either intact or had vestibular lesions (VL), sinoaortic denervation (SAD), or VL plus SAD (VL + SAD). The rats were exposed to 3 G in dorsoventral axis by centrifugation for 3 min. In rats in which neither reflex was functional (VL + SAD group), RSNA did not change, but the AP showed a significant decrease (-8 ± 1 mmHg vs. baseline). In rats with a functional baroreflex, but no VSR (VL group), the AP did not change and there was a slight increase in RSNA (25 ± 10% vs. baseline). In rats with a functional VSR, but no baroreflex (SAD group), marked increases in both AP and RSNA were observed (AP 31 ± 6 mmHg and RSNA 87 ± 10% vs. baseline), showing that the VSR causes an increase in AP in response to gravitational stress; these marked increases were significantly attenuated by the baroreflex in the intact group (AP 9 ± 2 mmHg and RSNA 38 ± 7% vs. baseline). In conclusion, AP is controlled by the combination of the baroreflex and VSR. The VSR elicits a huge pressor response during gravitational stress, preventing hypotension due to blood redistribution. In intact rats, this AP increase is compensated by the baroreflex, resulting in only a slight increase in AP.

scholarly journals Ameliorative effect of apelin-13 against renal complications in L-NAME-induced preeclampsia in rats

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11110
Author(s):  
Reham Z. Hamza ◽  
Abdel Aziz A. Diab ◽  
Mansour H. Zahra ◽  
Ali K. Asalah ◽  
Mai S. Attia ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Histopathological Examination ◽  
Female Rats ◽  
Serum Urea ◽  
Pregnant Rats ◽  
Arterial Blood ◽  
Total Urine

Pre-eclampsia (PE) accompanying acute liver and kidney injury has remained a master cause of both fetal and maternal mortality and morbidity. Vasoactive mediators, oxidative stress and inflammatory imbalanceshave an important role in PE pathogenesis. Apelin is an adipokine that improves endothelial dysfunction; has anti-inflammatory and antioxidant effects; moreover, its level reduced during PE. This study aimed to explore the effects of apelin-13 administration on preeclampsia-associated renal dysfunction and proteinuria. Thirty-three pregnant female rats were divided into three groups; group: 1 (normal pregnant rats), group: 2 (preeclamptic rats); where rats were injected subcutaneously with 75 mg L-NAME/ kg body weight/day beginning from 9th to 20th day of pregnancy andgroup 3 (apelin-13 treated preeclamptic rats); In which L-NAME-induced preeclamptic rats were subcutaneously injected with 6 × 10−8 mol apelin-13/kg body weight/twice daily starting from 6th to 20th day of pregnancy. In all groups, mean arterial blood pressure, total urine protein, serum urea, creatinine, nitric oxide (NO), endothelin-1 (ET-1), interleukin–6 (IL-6) and malondialdhyde (MDA) were measured. Histopathological examination of kidney tissues was also done. preeclamptic rats showed significantly increased mean arterial blood pressure, total urine proteins, serum urea, creatinine, ET-1, IL-6, and MDA, but revealed a significantly decreased serum NO level. On the other hand, apelin treatment significantly improved these parameters together with amelioration of kidney histoarchitecture in the treated group. In conclusion, apelin may be a potentially curative candidate for prohibiting kidney damage and have a therapeutic benefit in PE rat models.

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