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At least 181 records · Page 10Linked to original sources
PubMed2002

Sympathetic blockade significantly improves cardiovascular alterations immediately after spinal cord injury in rats.

Immediately after an experimental spinal cord injury (SCI) in rats, there is a large fall in mean arterial pressure (MAP) and heart rate (HR), followed by an abrupt increase in MAP. To better understand the mechanism involved in these early cardiovascular alterations, we tested the effect of treatment with ganglionic and sympathetic blockers in anesthetized rats subjected to T-5 SCI. Fall in MAP was partially diminished by propranolol and pentolinium, while increase in MAP was abolished by propranolol and pentolinium. Adrenalectomy did not diminish the fall in MAP and HR, however, the increase in MAP was significantly reduced. Likewise, propranolol and pentolinium completely abolished the effects in HR. These data suggest that the early cardiovascular alterations secondary to SCI results from an increased parasympathetic activity and a sympathetic withdrawal.

Adrenergic beta-Antagonists↗
PubMed1998

Central administration of a nitric oxide synthase inhibitor causes pressor responses via the sympathetic nervous system and the renin-angiotensin system in Wistar rats.

The central roles of nitric oxide (NO) in regulations of the blood pressure and heart rate were examined in anesthetized rats. Intracerebroventricular (i.c.v.) injection of Nomega-nitro-L-arginine methyl ester (L-NAME) caused dose-dependent increase in the blood pressure and heart rate. The pressor response of the blood pressure to L-NAME (2 micromol, i.c.v.) was reduced by L-arginine (5 micromol, i.c.v). Pretreatment with a ganglionic blocker, pentolinium (10 mg/kg, i.v.), significantly inhibited both pressor responses induced by L-NAME (2 micromol, i.c.v). The later pressor response of the blood pressure to L-NAME was also inhibited by the angiotensin II AT-1 blocker losartan (10 mg/kg, i.v). These results suggest that the response of the blood pressure to L-NAME is mediated by both the sympathetic nervous system and the renin-angiotensin system.

Animals↗
PubMed2002

Chronic central infusion of orexin-A increases arterial pressure in rats.

We determined the cardiovascular responses as well as food and water intakes to chronic intracerebroventricular administration of orexin-A and orexin-B for 14 days in conscious rats. Chronic intracerebroventricular infusion of orexin-A (50 pmol/h) elicited a significant increase in systolic blood pressure on the third day (+15.6 +/- 2.9 mm Hg), and during the continuous intracerebroventricular infusion of orexin-A the blood pressure returned to the baseline levels at day 14. In contrast, chronic intracerebroventricular infusion of orexin-B (50 pmol/h) failed to change systolic blood pressure during the 14 days of experimental periods. Chronic intracerebroventricular infusions of neither orexin-A nor orexin-B changed urinary catecholamine excretions, food and water intakes, and urine volumes at 7 and 14 days of infusion periods. Mean arterial pressure directly measured at 14 days did not differ among the groups of orexin-A, orexin-B, and artificial cerebrospinal fluid treatments. Both intravenous injections of pentolinium (5 mg/kg), a ganglion blocking agent, and CV-11974 (0.05 mg/kg), an AT(1) receptor antagonist, decreased arterial pressure; however, these responses were not different among the groups. These results suggest that central orexin-A participates in the short-term regulation of blood pressure; however, the contributions of central orexins to the long-term regulations of blood pressure, sympathetic nervous system, and appetite may be little.

Animals↗
PubMed1985

Interactions between neural mechanisms, the renin-angiotensin system and vasopressin in the maintenance of blood pressure during water deprivation: studies in Long Evans and Brattleboro rats.

1. Plasma volumes and cardiovascular status were assessed in rats with a congenital deficiency in hypothalamic vasopressin (Brattleboro strain) and in the parent strain (Long Evans), in water-replete and water-deprived states. 2. Water-replete Brattleboro rats were not hypovolaemic; water deprivation (14 h in Brattleboro rats, 53 h in Long Evans rats) produced similar percentage reductions in plasma volumes in the two groups. 3. In the water-replete state, cardiovascular variables were similar in Long Evans and Brattleboro rats. Inhibition of ganglionic transmission (with pentolinium) or of the renin-angiotensin system (with captopril), separately, did not have a greater effect on blood pressure in Brattleboro rats than in Long Evans rats. Recovery from hypotension caused by pentolinium was characterized by large swings in blood pressure in both groups of rats. These pressor episodes were abolished by administration of captopril to Brattleboro rats. After administration of pentolinium and captopril to Long Evans rats there was a substantial, although intermittent, recovery in blood pressure that was abolished by an antagonist of the cardiovascular actions of vasopressin. 4. In the water-deprived state, blood pressures were similar in Long Evans and Brattleboro rats; both groups showed an elevation in diastolic blood pressure relative to the water-replete state. After administration of pentolinium, there was a more marked recovery in blood pressure than was seen in the water-replete state. Administration of captopril alone had a slightly greater effect on blood pressure in Long Evans rats in the water-deprived, compared with the water-replete, state. However, in the former condition, Brattleboro rats showed a profound and progressive hypotension in response to captopril, indicating an indispensable role for the renin-angiotensin system in the maintenance of blood pressure in these animals during water deprivation. 5. Only when the renin-angiotensin system and neural activity were inhibited did vasopressin express its full, independent, pressor potential in Long Evans rats. However, evidence was obtained that vasopressin may exert important effects on cardiovascular regulation via neural mechanisms and through interactions with the renin-angiotensin system.

Animals↗
PubMed1986

The contribution of the autonomic nervous system, the renin-angiotensin system and vasopressin to the maintenance of arterial blood pressure in adrenalectomized Wistar rats.

Factors contributing to the maintenance of resting arterial blood pressure in sham-operated and adrenalectomized rats were assessed 14 weeks after operation; some animals were given 1% NaCl to drink throughout, and some animals were given sodium-free water instead of 1% NaCl for 2 days before the experiment. Inhibition of the renin-angiotensin (ANG) system (with captopril) and of the cardiovascular actions of vasopressin [with 1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid),8-D-arginine vasopressin (d(CH2)5DAVP)] had no hypotensive effects in sham-operated rats under any conditions, but antagonism of nicotinic ganglionic transmission (with pentolinium) caused a prompt fall in blood pressure. During combined administration of captopril, d(CH2)5DAVP and pentolinium to sham-operated rats, there was no significant recovery of blood pressure. Adrenalectomized rats drinking 1% NaCl showed a marked hypotension and tachycardia in response to captopril, but d(CH2)5DAVP had little effect, whether administered before or after captopril. Addition of pentolinium rendered these animals more hypotensive than the sham-operated rats. Adrenalectomized rats drinking sodium-free water for 2 days were hypotensive and blood pressures were lowered further by d(CH2)5DAVP or captopril under these conditions; there was no accompanying tachycardia. The results indicate that, in chronically adrenalectomized rats drinking 1% NaCl, blood pressure is maintained by autonomic nervous and renin-ANG systems with no discernible contribution from the peripheral cardiovascular actions of vasopressin. However, the latter contribute importantly to the support of blood pressure when the adrenalectomized rats are rendered hypovolaemic and hypotensive by substitution of sodium-free water to drink.

Adrenalectomy↗
PubMed1989

Evidence that intravenous morphine stimulates central opiate receptors to increase sympatho-adrenal outflow and cause hypertension in conscious rabbits.

1. In conscious rabbits, intravenous morphine caused hypertension, bradycardia, hyperglycaemia and increased plasma adrenaline and noradrenaline. These effects were prevented by ganglionic blockade with pentolinium. 2. The cardiovascular responses to morphine were not altered by pretreatment with a vasopressin V1-receptor antagonist. 3. After bilateral adrenalectomy morphine caused a similar rise in noradrenaline but no increase in adrenaline. The rise in blood pressure was attenuated and the hyperglycaemia was abolished. 4. Adrenaline infused intravenously to mimic the levels that occurred after morphine caused a similar degree of hyperglycaemia but only a small increase in blood pressure. 5. Pretreatment with intracerebroventricular naloxone prevented the morphine-induced hypertension, hyperglycaemia, increase in plasma catecholamines, respiratory depression and sedation. 6. These results demonstrate that, in conscious rabbits, intravenous morphine causes hypertension by increasing sympathetic vasoconstrictor nerve activity and elevating plasma adrenaline levels; the latter alone produces the hyperglycaemia. Vasopressin release is not involved in the hypertensive response to morphine. The effects of morphine appear to result from stimulation of central opiate receptors leading to enhanced sympathoadrenal outflow.

Adrenalectomy↗
PubMed1995

Contribution of vascular nitric oxide to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats.

1. The aim of this study was to clarify the extent to which vascular nitric oxide contributes to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats. 2. The contribution of vascular nitric oxide to maintenance of blood pressure was estimated by measuring the pressor response to an intravenous injection of nitric oxide synthase inhibitor, N omega-L-arginine methyl ester, given after serial injections of captopril, vasopressin V1-receptor antagonist (V1-antagonist) and ganglion blocker (pentolinium) in conscious spontaneously hypertensive and Wistar Kyoto rats aged 20-28 weeks. To estimate the 'amplifier property' of hypertrophied vasculature in spontaneously hypertensive rats, which is known to modulate pressor responses, the lower blood pressure plateau after serial injections of captopril, V1-antagonist and pentolinium and the maximum blood pressure elicited by subsequent injection of increasing doses of phenylephrine were also measured. 3. The serial injections of captopril, V1-antagonist and pentolinium decreased mean arterial pressure from 164 +/- 9 mmHg to 67 +/- 2 mmHg and from 117 +/- 2 mmHg to 49 +/- 1 mmHg in spontaneously hypertensive and Wistar Kyoto rats respectively. The subsequent injection of N omega-L-arginine methyl ester restored mean arterial pressure almost to its control levels in both spontaneously hypertensive and Wistar Kyoto rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

The acute cardiovascular actions of intravenous thyrotrophin releasing hormone (TRH) in man are mediated by non-catecholaminergic mechanisms.

1. Intravenous bolus doses of thyrotrophin releasing hormone (TRH, 50-1000 micrograms) caused statistically significant, non-dose dependent and transient rises in blood pressure, heart rate and plasma catecholamines in healthy young males. 2. Mean peak incremental rises in systolic blood pressure (mean +/- s.e. mean) following 50, 200 and 500 micrograms TRH were 14.3 +/- 2.9 mmHg, 15.7 +/- 3.2 mmHg and 17.1 +/- 3.9 mmHg respectively (all P < 0.05 vs placebo). Mean incremental rises in heart rate for the three doses of TRH were 8.2 +/- 2.2 beats min-1, 7.1 +/- 1.8 beats min-1, and 10.7 +/- 2.9 beats min-1 respectively (all P < 0.05 vs placebo). 3. Following the 50 micrograms and 1000 micrograms doses of TRH, plasma noradrenaline and adrenaline rose significantly (P < 0.05) between 4 and 8 min. Mean +/- s.e. mean incremental plasma noradrenaline rise following 50, 200 and 100 micrograms TRH were 0.4 +/- 0.13 nmol 1(-1), 0.37 +/- 0.21 nmol 1(-1) and 0.41 +/- 0.18 nmol 1(-1) respectively. Mean +/- s.e. mean incremental rise in adrenaline for the 50, 200 and 1000 micrograms dose were 0.13 +/- 0.04 nmol 1(-), 0.08 +/- 0.03 nmol 1(-1), and 0.11 +/- 0.05 nmol 1(-1) respectively. 4. Following administration of the ganglion blocking drug pentolinium (5 mg) the incremental systolic blood pressure and heart rate rises following 500 micrograms TRH alone 16.6 +/- 2.8 mmHg and 10.4 + 3.1 beats min-1 respectively. 5. The rises in plasma noradrenaline and adrenaline following TRH were attenuated by prior ganglion blockade. 6. alpha-Adrenoceptor blockade with thymoxamine (0.3 mg kg-1 bolus + 0.3 mg kg-1 h-1 infusion), singly and combined with intravenous propranolol (10 mg i.v. over 10 min), did not alter the pressor or tachycardic effects of 500 micrograms TRH. 7. In conclusion, although plasma noradrenaline rises following i.v. TRH, suggesting activation of the sympathetic nervous system, this effect is not responsible for the pressor response to TRH, which appears to be due to either a direct vasoconstrictive effect on the peripheral resistance vessels or a direct inotropic/chronotropic effect on the heart.

Adrenergic Antagonists↗
PubMed1997

DMPP-evoked increases in postganglionic sympathetic nerve activity and blood pressure occurs by two mechanisms in the rat.

1. Intravenous administration of the ganglionic nicotinic receptor agonist DMPP (1,1-dimethyl-4-phenylpiperazinium iodide) into urethane-anaesthetized rats evoked dose-dependent increases in mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). 2. The ganglionic nicotinic receptor antagonists pentolinium and hexamethonium either alone or combined did not inhibit the increase in RSNA and MAP evoked by 50 to 200 micrograms kg-1 doses of DMPP. The increase in renal sympathetic nerve activity evoked by DMPP occurred as a brief burst in firing. 3. The increase in MAP, but not RSNA, evoked by DMPP in the presence of pentolinium was inhibited by the selective alpha 1-adrenergic receptor antagonist prazosin. 4. The non-selective alpha-adrenoceptor and NPY receptor antagonist benextramine also inhibited the increase in MAP without inhibiting the increase in RSNA. Surprisingly, the combination of benextramine and pentolinium, or benextramine and hexamethonium, completely blocked the DMPP-evoked increase in RSNA and thus the increase in MAP. 5. The uptake1 antagonist desipramine combined with pentolinium did not affect the DMPP-evoked increases in MAP or RSNA when compared to the responses evoked in the presence of pentolinium alone. 6. Adding the selective M1 muscarinic receptor antagonist telenzepine to pentolinium and prazosin did not inhibit the increase in RSNA evoked by a 100 micrograms kg-1 dose of DMPP. 7. While the DMPP-evoked increase in MAP in the presence of ganglionic nicotinic receptor antagonists is primarily dependent upon activation of alpha 1-adrenoceptors, the increase in RSNA occurs via activation of ganglionic nicotinic receptors and activation of a mechanism susceptible to blockade by benextramine.

Adrenergic Uptake Inhibitors↗
PubMed1998

Cardiovascular responses evoked by carbachol microinjection into the posterior hypothalamus involves ganglionic nicotinic and muscarinic mechanisms.

1. Microinjection of the cholinergic agonist carbachol (3.3, 5.5 and 13.2 nmol) into the posterior hypothalamic nucleus of conscious rats evokes a dose-dependent increase in blood pressure. The pressor response evoked by the lower doses of carbachol was attenuated by pretreatment with the ganglionic nicotinic receptor antagonist pentolinium (10 mg kg(-1), i.v.) while blockade of V1-vasopressin receptors with [d(CH2)5Tyr(Me)]AVP (20 microg kg(-1), i.v.) reduced the pressor response evoked by the highest dose. 2. The combination of pentolinium and the muscarinic receptor antagonist methylatropine (2 mg kg(-1), i.v.) completely blocked the response evoked by the lower doses while the addition of [d(CH2)5Tyr(Me)]AVP to these two antagonists was required for further inhibition of the pressor response to the highest dose of carbachol. Bilateral adrenal demedullation did not affect the pressor response evoked by 5.5 or 13.2 nmol of carbachol. 3. Treatment of intact and adrenal demedullated rats with pentolinium after the pressor response to 13.2 nmol of carbachol was underway reversed the pressor response, but not to the same degree as that provided by the combination of pentolinium and methylatropine, or pentolinium and [d(CH2)5Tyr(Me)]AVP. 4. Methylatropine or [d(CH2)5Tyr(Me)]AVP caused a slight reversal of the carbachol-induced pressor response once it was underway in intact rats. Methylatropine given before or after pentolinium worked with the pentolinium to completely reverse the response. Methylatropine given alone reversed the bradycardia evoked by carbachol to a tachycardia which itself was antagonized by subsequent treatment with pentolinium. 5. These results suggest that the pressor response evoked by carbachol microinjection into the posterior hypothalamic nucleus of conscious rats involves sympathoexcitation and vasopressin release. The sympathoexcitation involves nicotinic and muscarinic receptors in autonomic ganglia.

Adrenal Medulla↗