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At least 217 records · Page 12Linked to original sources
PubMed2002

The altered balance between sympathetic nervous system and nitric oxide in salt hypertensive Dahl rats: ontogenetic and F2 hybrid studies.

OBJECTIVE: We have demonstrated earlier that the nitric oxide (NO) system is not able to counterbalance effectively the hyperactivity of the sympathetic nervous system (SNS) in salt hypertension of young Dahl rats in which augmented superoxide anion formation lowers NO bioavailability. The aim of the present study was to determine whether SNS hyperactivity and/or relative NO deficiency are also present in salt hypertension elicited in adult Dahl rats, and whether they are associated with blood pressure (BP) in the F2 population of Dahl rats. DESIGN AND METHODS: The contribution of major vasoactive systems [renin-angiotensin system (RAS), SNS and NO] and superoxide anions to BP maintenance was studied in SS/Jr rats in which salt hypertension was induced either in adulthood or in youth (8% NaCl diet from the age of 12 or 4 weeks). The contribution of particular vasoactive systems was also investigated in 122 young salt-loaded F2hybrids [derived from salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) Dahl rats] which were fed a high-salt diet (8% NaCl) for 6 weeks after weaning. Mean arterial pressure (MAP) was measured in conscious animals subjected to acute consecutive blockade of RAS (captopril 10 mg/kg i.v.), SNS (pentolinium 5 mg/kg i.v.) and NO synthase (l-NAME 30 mg/kg i.v.). RESULTS: Dahl rats with salt hypertension induced in adulthood were also characterized by enhanced pentolinium-induced BP fall (DeltaMAPpento), but their residual BP (recorded after the blockade of both RAS and SNS) was unaltered, in contrast to its elevation seen in young salt-hypertensive rats. The BP rise after NO synthase inhibition by l-NAME (DeltaMAPL-NAME), which was substantially greater in adult than in young hypertensive rats, was not enhanced by superoxide scavenging with tempol in adult hypertensive animals, in which this drug elicited a moderate BP reduction only. Basal MAP of young salt-loaded F2 hybrids was positively associated not only with DeltaMAPpento (P < 0.0001) and residual BP (P < 0.001) but also with DeltaMAPL-NAME (P < 0.001). The slope of the relationship between basal BP and pentolinium-induced BP changes was steeper than that between basal BP and BP changes elicited by l-NAME. The positive correlation of basal BP with DeltaMAPpento/DeltaMAPL-NAME ratio (P < 0.01) indicates that an altered balance between sympathetic vasoconstriction and NO-dependent vasodilation was associated with high blood pressure, even in the F2 population of Dahl rats. CONCLUSIONS: A comparison of young and adult salt-hypertensive Dahl rats stressed the importance of increased residual BP and relative NO deficiency for the severity of hypertension, because these two alterations were absent in a less-pronounced form of salt hypertension elicited in adulthood. The findings obtained in our young salt-loaded F2 population also confirm the major importance of both sympathetic hyperactivity and relative NO deficiency for the maintenance of salt hypertension in Dahl rats.

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PubMed2003

Central cardiovascular action of urotensin II in conscious rats.

OBJECTIVE: To examine the central cardiovascular action of urotensin II in conscious rats. METHODS: Intracerebroventricular (ICV) injections of urotensin II (1 and 10 nmol) were carried out in conscious Wistar rats. The effects of intravenous (i.v.) urotensin II (10 nmol) were also determined. RESULTS: The ICV injection of urotensin II at a dose of 1 nmol did not alter the arterial pressure or heart rate significantly, while 10 nmol urotensin II increased the arterial pressure and heart rate. The mean arterial pressure at 5 min of ICV urotensin II was 121 +/- 4 mmHg, which was significantly higher than that obtained by ICV injection of artificial cerebrospinal fluid (107 +/- 3 mmHg, P <0.05). In addition, significant increases in heart rate were observed 5-15 min after ICV urotensin II. Pre-treatment with pentolinium (5 mg/kg, i.v.) significantly attenuated the increases in mean arterial pressure (20 +/- 3 versus 8 +/- 2 mmHg, P <0.01) and heart rate (78 +/- 18 versus 7 +/- 5 beats/min, P <0.05) induced by ICV urotensin II. On the other hand, i.v. injection of urotensin II (10 nmol) elicited a depressor response associated with tachycardia; mean arterial pressure 5 min after injection was significantly lower in the urotensin II-injected rats (89 +/- 5 mmHg) than in the control rats (102 +/- 2 mmHg, P <0.05), and the heart rate was significantly higher in the former (402 +/- 11 versus 360 +/- 9 beats/min, respectively, P <0.05). CONCLUSIONS: Central urotensin II produces pressor and tachycardic responses through sympathetic activation, while peripheral urotensin II exerts a vasodilation-mediated depressor response in conscious rats.

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PubMedDate not supplied

The effect of intravenous administration of GABA and brain extracts on blood pressure in the rat.

1. A rat bioassay was used to study pressor substances in brain extracts. 2. A compound with pressor activity in pentolinium-treated rats was extracted from brain, purified using Dowex, Sephadex electrophoresis and identified as gamma-aminobutyric acid (GABA) by HPLC and mass spectrometry. 3. Intravenous GABA (1-5 microgram) or brain extracts caused a dose dependent decrease in blood pressure in pentobarbitone-anaesthetized rats. 4. After ganglion blockade with pentolinium (2 mg/kg subcutaneously), GABA or brain extracts cause a dose dependent increase in rat blood pressure. 5. This pressor effect is reduced by alpha- and beta-blockers (intravenous phentolamine, 0.5 mg/kg and propranolol, 0.05 mg/kg). 6. It is concluded that GABA causes a fall in blood pressure by a central mechanism and ganglion blockade unmasks a pressor effect.

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PubMedDate not supplied

Studies in the rat on endralazine, a new antihypertensive drug structurally related to hydralazine.

1. The effects on blood pressure, heart rate and plasma renin activity of a new hydralazine congener, endralazine, were evaluated in anaesthetized rats. Dose-response relationships for endralazine, hydralazine and diazoxide, administered intravenously, were compared, and the interactions of endralazine with the ganglionic blocking agent, pentolinium, or with adrenaline, noradrenaline and angiotensin II were examined. 2. In the dose range 0.05 to 1.0 mg/kg, endralazine produced prompt dose-related reductions in systolic and diastolic blood pressure, with relatively little effect on heart rate. The drug had a pronounced dose-related renin stimulating effect. 3. Endralazine retained approximately 80% of its hypotensive activity after pretreatment with pentolinium, and caused no significant attenuation of pressor responses to adrenaline, noradrenaline or angiotensin II. 4. Endralazine was an effective hypotensive agent, with a prompt onset of action, a prolonged and stable effect, and a potency at least twice that of hydralazine and 20 to 25 times that of diazoxide. The data are consistent with a predominantly direct vasodilator mode of action.

Animals↗
PubMed1993

Vasopressin compensates for acute loss of sympathetic pressor tone in spontaneously hypertensive rats.

1. The aim of this study was to examine the pressor response of vasopressin (AVP) to an acute fall in blood pressure induced by ganglion blockade. 2. Aortic catheters were implanted in spontaneously hypertensive rats (SHR) stroke-prone SHR (SHRSP), normotensive Wistar-Kyoto (WKY), black-hooded Wistar (BHW) and Sprague-Dawley (SD) rats, aged 5-7 weeks and 7-9 months, for direct measurement of mean arterial pressure (MAP) under conscious, resting conditions. The ganglion blocking agent pentolinium was administered intra-arterially, followed by an AVP receptor antagonist specific for the pressor effect of AVP. The basal level of MAP attained with each drug was recorded. 3. In the adult SHR and SHRSP with established hypertension, acute ganglion blockade caused MAP to fall to a similar extent as in WKY, suggesting that the level of sympathetic pressor tone was similar in all three strains. Administration of the AVP antagonist alone did not affect resting MAP. During ganglion blockade, however, it caused a further reduction of MAP in WKY, SHR and SHRSP, the magnitude of which was greater in the hypertensive strains. After both drugs, the total fall in MAP and the residual MAP were significantly greater in the hypertensive rats. 4. In young rats, AVP had little effect on MAP, even during ganglion blockade. The residual level of MAP after both drugs was greater in the hypertensive strains. 5. The extent to which AVP can compensate for an acute fall in MAP increases with age and the development of hypertension. This tends to mask the loss of sympathetic mediated pressor tone after ganglion blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed2005

Pressor and tachycardic responses evoked by microinjections of L-glutamate into the medial prefrontal cortex of unanaesthetized rats.

The ventral medial prefrontal cortex (vMPFC) is involved in central cardiovascular control. In the present study, we studied the cardiovascular effects of injections of L-glutamate into the vMPFC of unanaesthetized rats and the mechanisms of these effects. Male Wistar rats were used and L-glutamate was microinjected in the vMPFC in a final volume of 200 nL. Microinjections of L-glutamate (9, 27, 81, 150 or 300 nmol) caused long-lasting, dose-related pressor and tachycardic responses in unanaesthetized rats. No differences were observed among cardiovascular responses when L-glutamate was injected into the three sub-areas that comprise the vMPFC, namely the prelimbic, the infralimbic and the dorsal peduncular cortices. No responses were observed when the dose of 81 nmol of L-glutamate was microinjected into surrounding structures such as the cingulate cortex area 1, the corpus callosum and the tenia tecta, indicating a predominant action on the vMPFC. The cardiovascular response to L-glutamate into the vMPFC was blocked by intravenous pretreatment with the ganglion blocker pentolinium (10 mg/kg, i.v.) or the beta1-adrenoceptor antagonist atenolol (1.5 mg/kg, i.v.), supporting the involvement of the cardiac sympathetic nervous system in the response to L-glutamate. Pretreatment with the muscarinic antagonist homatropine methyl bromide (1 mg/kg, i.v.) reduced the latency to the onset of the pressor and tachycardic responses to L-glutamate injected into the vMPFC without significant effects on response duration or maximum effect. We conclude that stimulation of the vMPFC with L-glutamate caused pressor and tachycardic responses in unanaesthetized rats, responses which were dependent on cardiac sympathetic nerve activation and were potentiated by blockade of peripheral muscarinic receptors.

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PubMed2005

Cardiovascular effects of noradrenaline microinjected into the dorsal periaqueductal gray area of unanaesthetized rats.

The periaqueductal grey area (PAG) is a mesencephalic region that is involved in the modulation of cardiovascular changes associated with behavioural responses. Among the neurotransmitters present in the PAG, noradrenaline (NA) is also known to be involved in central nervous system cardiovascular regulation. In the present study we report the cardiovascular effects of the microinjection of NA into the dorsal portion of the PAG (dPAG) of unanaesthetized rats and the peripheral mechanism involved in their mediation. Injection of NA in the dPAG of unanaesthetized rats evoked a dose-dependent pressor response accompanied by bradycardia. The magnitude of the pressor responses was higher at more rostral sites in the dPAG and decreased when NA was injected into the caudal portion of the dPAG. The responses to NA were markedly reduced in urethane-anaesthetized rats. The pressor response was potentiated by i.v. pretreatment with the ganglion blocker pentolinium and blocked by i.v. pretreatment with the vasopressin antagonist dTyr(CH2)5(Me)AVP. The results suggest that activation of noradrenergic receptors within the dPAG can evoke pressor responses, which are mediated by acute vasopressin release.

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PubMed1975

The influence of vesical distension on urethral resistance to flow: the collecting phase.

Using female dogs, changes in the urethral pressure profile in response to vesical distension were studied. It was noted that during the collecting phase there was an increase in the amplitude of the profile tracing. These experiments revealed that this increase is not mediated through an autonomic reflex and does not reflect a significant enhancement of alpha-adrenergic activity. These changes are mainly due to increased tension of the urethral muscle, secondly to detrusor stretch.

Animals↗
PubMed1975

The influence of vesical distension on urethral resistance to flow: the expulsion phase.

The influence of vesical distension of the urethral pressure profile was studied in female dogs, using a model in which the bladder and urethra were separated. There was a reduction in the urethral resistance involving its smooth and striated muscle components. This reduction was completely blocked by ganglion blocking agents. Atropine did not influence these changes. Propranolol could only partially block this reflex. The other possible mechanisms that could be involved were discussed.

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PubMed1982

Exogenously stimulated gastric secretion in dogs after ganglion and sympathetic blockade and antral acidification.

1 In conscious dogs with gastric fistulae, Heidenhain pouches and in some cases, innervated pyloric pouches, ganglionic blockade augmented Heidenhain pouch acid secretion only if the gastric fistula remained closed in animals receiving pentagastrin. 2 Ganglionic blockade depressed methacholine-stimulated acid and pepsin secretion from the Heidenhain pouch whether or not the fistula was open. 3 Acidification of the antral pouch consistently augmented the acid and pepsin secretion from the Heidenhain pouch when either pentagastrin or methacholine was the stimulus. Ganglionic blockade prevented this.

Animals↗
PubMed1958

The peripheral action of hexamethonium and of pentolinium.

The influence of hexamethonium and pentolinium on the responses of certain peripheral effector cells to adrenaline, noradrenaline or postganglionic stimulation was studied in the cat. The actions of adrenaline and noradrenaline on the blood vessels of a limb and of adrenaline and postganglionic stimulation on the nictitating membrane were increased after the administration of hexamethonium and pentolinium. This effect was considered to be due to sensitization of the peripheral effector cells. The possible significance of these findings is discussed.

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