Hypothalamic α-adrenergic blockade modifies drinking and blood pressure responses to central angiotensin II in conscious rats

1988 ◽  
Vol 66 (10) ◽  
pp. 1270-1277 ◽  
Author(s):  
D. L. Jones
Keyword(s):  
Angiotensin Ii ◽  
Adrenergic Receptors ◽  
Adrenergic Blockade ◽  
Drinking Response ◽  
Pressor Responses ◽  
Awake Rat ◽  
Rostral Hypothalamus ◽  
Blood Pressure Responses ◽  
Β Adrenergic Receptors ◽  
Dose Dependent

These experiments investigated in the awake rat the involvement of noradrenergic projections to the rostral hypothalamus in the drinking and pressor responses elicited by intracerebroventricular (i.c.v.) injections of 25 ng of angiotensin II. Phentolamine mesylate in doses of 2.5–125 μg injected into the rostral hypothalamus produced a dose-dependent depression of both the drinking and pressor responses elicited by i.c.v. administration of angiotensin II. A paradoxical increase in heart rate was associated with a decrease in pressor responses with increasing doses of phentolamine. This response was due to tissue injections, since pretreatment by injecting 12.5 μg of phentolamine into the ventricle did not block either the cardiovascular or drinking responses to i.c.v. injections of angiotensin II. Yohimbine (0.33–3.3 μg), DL-propranolol (25 μg), and atenolol (25 μg) did not, but prazosin (0.7 μg) did significantly alter the pressor responses. Although yohimbine also was without effect on drinking, prazosin reduced the drinking responses. These results suggest that α1-adrenergic receptors in the rostral hypothalamus are involved in the control of both the drinking and pressor responses elicited by i.c.v. injections of angiotensin II. In the case of propranolol and atenolol, β-adrenergic receptors altered only the drinking response in a nonspecific manner by eliciting competing behaviors. Whether they are involved in modifying the drinking response only remains to be demonstrated.

Separation of drinking and pressor responses to central angiotensin by monoamines

1981 ◽  
Vol 240 (1) ◽  
pp. R106-R113 ◽  
Author(s):  
A. Camacho ◽  
M. I. Phillips
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Adrenergic Blockade ◽  
Serotonin Agonist ◽  
Drinking Response ◽  
Pressor Responses ◽  
Angiotension Ii ◽  
Alpha Receptors

This study investigated the neurotransmitters involved in the increase in blood pressure and drinking produced when angiotension II is injected intraventricularly (ivt). Using pharmacologic manipulations of the monoamines norepinephrine, dopamine, and serotonin it has been possible to separate the pressor response from dipsogenic responses to angiotension II. Alpha-adrenergic blockade with phentolamine restricted to the brain blocked the pressor response to angiotensin II in a dose-related manner, while drinking remained unaffected. Norepinephrine alone, injected into the ventricles elevated blood pressure, but did not produce drinking. The norepinephrine effect was also blocked by phentolamine by the same ventricular route. Other monoamines were not involved. Dopamine alone did not produce thirst. Cardiovascular effects with dopamine were observed only with large doses. The dopaminergic agonist apomorphine produced no change in blood pressure or drinking. Reduction of central serotonin stores by p-chlorophenylalanine intraperitoneally or 5,7-dihydroxytryptamine intraventricularly had no effect on the pressor or dipsogenic effects of angiotensin II. The serotonin agonist N,N-dimethyl-5-methoxytryptamine ivt did not produce a rise in blood pressure or drinking. It is concluded that the pressor effect of angiotensin II, but not the drinking effect is mediated by noradrenergic stimulation of alpha-receptors. The drinking response does not appear to be mediated by the monoamines.

Mediation of isoproterenol-induced thirst in rats by β2-adrenergic receptors

1978 ◽  
Vol 56 (3) ◽  
pp. 465-470 ◽  
Author(s):  
M. J. Katovich ◽  
M. J. Fregly
Keyword(s):  
Water Intake ◽  
Adrenergic Receptors ◽  
Subcutaneous Administration ◽  
Female Rats ◽  
Acute Administration ◽  
Drinking Response ◽  
Adrenergic Antagonist ◽  
Blocking Activity ◽  
Β Adrenergic Receptors ◽  
Adrenergic Blocking

Isoproterenol-induced thirst in rats has been attributed to the activation of β-adrenergic receptors. Since these receptors can be further differentiated pharmacologically into β1 and β2 types, experiments were performed using several β-adrenergic agonists and antagonists to determine the receptor type initiating the isoproterenol-induced thirst. The β1- and β2-adrenergic antagonist, d,l-propranolol (1 mg/kg, ip), blocked the increase in water intake usually accompanying acute subcutaneous administration of isoproterenol (25 μg/kg) to female rats. Since l-propranolol is known to stabilize membranes and to possess anesthetic-like properties, d-propranolol was also used. This isomer has little β-adrenergic-blocking activity but possesses anesthetic-like activity. Administration of d-propranolol (1 mg/kg, ip) failed to affect the drinking response to acute administration of isoproterenol (25 μg/kg). Practolol (125 mg/kg), a β1-adrenergic antagonist with little anesthetic properties, also had no effect on water intake of isoproterenol-treated rats. Butoxamine, a selective β2-adrenergic antagonist, attenuated the drinking response to isoproterenol. Salbutamol (150 μg/kg), a β2-adrenergic agonist, mimicked the effect of isoproterenol on water intake. These results are consistent with the suggestion that β2-adrenergic receptors mediate the isoproterenol-induced thirst in rats.

Propranolol Block of Adrenaline-Induced Hypophosphataemia in Man

1970 ◽  
Vol 38 (2) ◽  
pp. 245-250 ◽  
Author(s):  
F. Massara ◽  
F. Camanni
Keyword(s):  
Blood Glucose ◽  
Adrenergic Receptors ◽  
Adrenergic Blockade ◽  
Plasma Lactate ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Β Adrenergic Receptors

1. The effect of propranolol on adrenaline- and insulin-induced hypophosphataemia was studied in man. 2. β-Adrenergic blockade with propranolol almost completely abolished and significantly inhibited adrenaline- and insulin-induced hypophosphataemia respectively; in addition, the drug clearly prevented the normally observed rise in plasma lactate, while causing only a slight change in blood glucose levels. 3. It is suggested that the fall in blood phosphate values induced by adrenaline and, in part, that caused by insulin, is mediated by β-adrenergic receptors.

Kainic acid lesions of the median preoptic nucleus: effects on angiotensin II induced drinking and pressor responses in the conscious rat

1988 ◽  
Vol 66 (8) ◽  
pp. 1082-1086 ◽  
Author(s):  
D. L. Jones
Keyword(s):  
Angiotensin Ii ◽  
Kainic Acid ◽  
Pressor Response ◽  
Cerebral Ventricle ◽  
Central Administration ◽  
Preoptic Region ◽  
Conscious Rat ◽  
Drinking Response ◽  
Pressor Responses ◽  
Lateral Cerebral Ventricle

Input to the nucleus medianus of the preoptic region has been suggested to be involved in both the drinking and pressor responses elicited by the central administration of angiotensin II. Evidence in support of this suggestion has been gained principally from electrical lesion experiments. This lesion procedure does not differentiate between the cells of the region and fibers coursing through the region. To test the hypothesis that cells in this region are involved in both the pressor and drinking responses elicited by central administration of angiotensin II, injections of kainic acid were made to induce lesions of the cells, while sparing fibers of passage. Drinking and blood pressure responses were determined pre- and post-lesion in the chronically instrumented awake rat. Injections of 50 ng angiotensin II in a 2-μL volume into a lateral cerebral ventricle of the conscious rat elicited pronounced drinking and pressor responses with a latency of 3–5 min. Lesions of the median preoptic region produced by injecting 1.0 μg of kainic acid in 0.25 μL for 15 s attenuated or blocked the drinking response and increased the latency to drink induced by central injections of angiotensin II. However, kainic acid lesions did not significantly alter the pressor responses produced by angiotensin II administration. These results suggest that cells in the median preoptic region are involved in the drinking response but do not participate in the pressor response elicited by angiotensin II administration into a lateral cerebral ventricle of the conscious rat.

Nonadrenergic mechanisms of cocaine-induced regional vascular responses in rats

1994 ◽  
Vol 72 (4) ◽  
pp. 335-343 ◽  
Author(s):  
Mark M. Knuepfer ◽  
Carrie A. Branch ◽  
David M. Wehner ◽  
Qi Gan ◽  
Dung Hoang
Keyword(s):  
Arterial Pressure ◽  
Local Anesthetic ◽  
Adrenergic Receptors ◽  
Regional Blood Flow ◽  
Pressor Response ◽  
Pulsed Doppler ◽  
Doppler Flowmetry ◽  
Pressor Responses ◽  
Induced Changes ◽  
Β Adrenergic Receptors

The pressor response to cocaine is a consequence of mesenteric vasoconstriction and hindquarters vasodilation as a result of activation of α1- and β-adrenergic receptors, respectively. In the present study, evidence for additional, nonadrenergic effects of cocaine-induced changes in regional blood flow was obtained using pulsed Doppler flowmetry in conscious rats. Cocaine produced dose-dependent initial peaks (within 1 min) in mean arterial pressure concomitant with an increase in hindquarters and mesenteric vascular resistance. The sustained, modest pressor response was associated with hindquarters vasodilation and bradycardia. The cocaine-induced vasodilation was enhanced by pretreatment with indomethacin (5 mg/kg), prevented by ibuprofen (12.5 mg/kg) or 3-amino-1-[m-(trifluoromethyl)-phenyl]-2-pyrazoline (BW755C, 10.5 mg/kg) pretreatment, and unaffected by meclofenamate administration (2.5 mg/kg). Equipotent local anesthetic doses of procaine produced equivalent hindquarters vasodilator responses and more modest pressor responses. Dial–urethane anesthesia did not affect hindquarters vasodilation in response to cocaine or procaine but did reduce the mesenteric vasoconstrictor and pressor responses. These data demonstrate that the cocaine-induced hindquarters vasodilation is not mediated solely by β-adrenergic receptors but is also dependent upon eicosanoids. Furthermore, the cocaine-induced vasodilation may be due, in part, to a direct local anesthetic effect but is not dependent upon a locomotor or behavioral stress induced increase in blood flow.Key words: anesthesia, eicosanoids, arterial pressure, hindquarters and mesenteric vascular resistances, pulsed Doppler flowmetry.

Effect of paraventricular nucleus lesions on drinking and pressor responses to ANG II

1988 ◽  
Vol 255 (6) ◽  
pp. R882-R887 ◽  
Author(s):  
M. B. Gutman ◽  
D. L. Jones ◽  
J. Ciriello
Keyword(s):  
Angiotensin Ii ◽  
Paraventricular Nucleus ◽  
Phosphate Buffer ◽  
Pressor Response ◽  
Neural Circuitry ◽  
Ang Ii ◽  
Drinking Response ◽  
Pressor Responses ◽  
Vehicle Injection ◽  
Bilateral Lesions

Experiments were done to investigate the contribution of cells of the paraventricular nucleus of the hypothalamus (PVH) to the drinking and pressor responses elicited by microinjection of angiotensin II (ANG II) into the subfornical organ (SFO) in the awake unrestrained rat. Microinjection of ANG II (5 eta g in 0.2 microliter) elicited drinking (7.1 +/- 0.7 ml in 15 min, n = 18) and pressor (19 +/- 1 mmHg, n = 17) responses. Bilateral lesions of the PVH by the administration of kainic acid (KA; 0.2 microgram in 0.2 microliter of phosphate buffer) resulted in the abolition of the drinking response (before, 7.8 +/- 1.8 ml in 15 min; after, 0 ml in 15 min, n = 6) and significant (P less than 0.05) attenuation of the pressor response (before, 15 +/- 1 mmHg; after, 5 +/- 2 mmHg, n = 5). Administration of 0.2 microliter of the phosphate buffer vehicle bilaterally into the PVH and KA into regions adjacent to the PVH had no significant effect on the drinking or pressor responses. KA injections into the PVH resulted in the loss of 70-80% of parvocellular cells in the posterodorsal component of the PVH compared with animals with KA injections into adjacent non-PVH tissue (n = 7) or vehicle injection into the PVH (n = 5). These results suggest that parvocellular cells of the PVH are an important component of the neural circuitry that mediates the drinking and pressor response to ANG II acting at the SFO.

Effects of intraventricular angiotensin II mediated by the sympathetic nervous system

1978 ◽  
Vol 235 (4) ◽  
pp. H392-H399 ◽  
Author(s):  
J. C. Falcon ◽  
M. I. Phillips ◽  
W. E. Hoffman ◽  
M. J. Brody
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Combined Treatment ◽  
Neural Activation ◽  
Water Drinking ◽  
Drinking Response ◽  
Before And After ◽  
Blood Pressure Responses ◽  
6 Hydroxydopamine ◽  
Prolonged Latency

Central effects of angiotensin II were studied in rats treated with adrenalectomy, chemical sympathectomy with intravenous 6-hydroxydopamine, or a combination of both. Unrestrained, unanesthetized rats were compared before and after one of the three treatments to determine water drinking and blood pressure responses to intracerebroventricular (ivt) injections of 50 and 500 ng angiotensin II (AII). Adrenalectomy alone did not alter either drinking or pressor response to AIIivt. Peripheral sympathectomy alone resulted in a prolonged latency for pressor response but did not significantly alter drinking response to AIIivt. Results obtained by combined treatment were not significantly different from results obtained by sympathectomy alone. There remained a pressor response to AIIivt after combined treatment. The adrenals do not appear to be involved in mediating pressor response to AIIivt. Furthermore, sympathetic neural activation alone causes the early pressor response to AIIivt. Finally, some other factor(s) in addition to sympathetic neural activation must contribute to the pressor response to AIIivt.

Trypsinization of bovine parathyroid cells abolishes Ca2+-regulated parathyroid hormone secretion

1989 ◽  
Vol 122 (1) ◽  
pp. 213-218 ◽  
Author(s):  
R. Muff ◽  
J. A. Fischer
Keyword(s):  
Protein Kinase C ◽  
Parathyroid Hormone ◽  
Protein Kinase ◽  
Adrenergic Receptors ◽  
Hormone Secretion ◽  
Dependent Manner ◽  
Kinase C ◽  
And Control ◽  
Β Adrenergic Receptors ◽  
Dose Dependent

ABSTRACT The secretion of parathyroid hormone (PTH) is inversely related to the extracellular Ca2+ concentration (Cae2+). To test the hypothesis that a Ca2+ sensor on the surface of parathyroid cells is involved in Ca2+-regulated PTH secretion, limited trypsinization of bovine parathyroid cells was carried out. Treatment with trypsin (1·1–10 mg/ml) inhibited, in a dose-dependent manner, PTH secretion stimulated by lowering Cae2+ from 2·0 to 0·5 mmol/l. In control cells, activation of protein kinase C with 12-O-tetradecanoylphorbol-13-acetate (TPA) enhanced PTH secretion at 2·0 mmol Cae2+/1 but not at 0·5 mmol Cae2+/1. In trypsinized cells, however, TPA enhanced PTH secretion at both 0·5 and 2·0 mmol Cae2+/1. Isoproterenol-stimulated PTH secretion was maintained in trypsinized cells, but reduced cyclic AMP production revealed that some β-adrenergic receptors were destroyed. The cytosolic free Ca2+ concentration (Cai2+), as measured with fura-2, was raised within seconds in response to increasing Cae2+ from 0·5 to 2·0 mmol/l and was then lowered within 1 min to a sustained plateau; the changes were the same in trypsinized and control cells. In conclusion, trypsinization of parathyroid cells abolished Ca2+-regulated PTH secretion without affecting Cai2+. Journal of Endocrinology (1989) 122, 213–218

Effect of angiotensin II in ventrolateral medulla of spontaneously hypertensive rats

1991 ◽  
Vol 260 (5) ◽  
pp. R977-R984 ◽  
Author(s):  
H. Muratani ◽  
D. B. Averill ◽  
C. M. Ferrario
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rat ◽  
Cardiovascular Response ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Pressor Responses ◽  
Wistar Kyoto ◽  
Dose Dependent

The spontaneously hypertensive rat (SHR) exhibits an enhanced activity of the peripheral sympathetic and brain renin-angiotensin systems. In the present experiments, we evaluated the cardiovascular response of angiotensin II (ANG II) microinjected in the rostral (RVLM) and the caudal (CVLM) ventrolateral medulla of age-matched (14-16 wk old) SHR and Wistar-Kyoto (WKY) rats. Responses of mean arterial pressure (MAP) and heart rate (HR) to microinjection of ANG II (5, 20 and 100 pmol) into histologically verified sites of the RVLM and CVLM were compared with those obtained by injections of the excitatory agent L-glutamate (2 nmol) at the same site. In both strains, ANG II elicited dose-dependent pressor responses in the RVLM and depressor responses in the CVLM, both of which peaked at a dose of 20 pmol. The magnitude of the fall in MAP produced by injections of ANG II into the CVLM were significantly (P less than 0.01) greater in SHR than in WKY group. In contrast, peak pressor responses elicited by injection of ANG II into the RVLM were of similar magnitude in the two groups. When compared with the MAP response produced by L-glutamate injections, responses to ANG II microinjection were slower in onset, and the latency to the peak response was longer. Ganglionic blockade with hexamethonium bromide prevented the effect of ANG II injection in the RVLM. This study provides evidence that ANG II acts as an excitatory agent at sites within the ventrolateral medulla that determine the vasomotor control of blood pressure in both normotensive and hypertensive rats.

scholarly journals Physiological regulation of MMPs and tPA/PAI in the arterial wall of rats by noradrenergic tone and angiotensin II

2011 ◽  
Vol 13 (1) ◽  
pp. 36-45 ◽  
Author(s):  
Houcine Dab ◽  
Rafik Hachani ◽  
Nedra Dhaouadi ◽  
Wassim Hodroj ◽  
Mohsen Sakly ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasminogen Activator ◽  
Adrenergic Receptors ◽  
Combined Treatment ◽  
Plasminogen Activator Inhibitor ◽  
Ang Ii ◽  
Plasminogen Activator Inhibitor 1 ◽  
Β Adrenergic Receptors ◽  
Pai 1

The interactions between the sympathetic nervous system (SNS) and angiotensin II (ANG II), and their direct effects in vitro on the enzymes involved in vascular extracellular matrix (ECM) degradation, were examined. Rats were treated with guanethidine, losartan or the combined treatments. mRNA, protein and activity of matrix metalloproteinase (MMP)-2 and MMP-9 and mRNA of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) were quantified in abdominal aorta (AA) and femoral artery (FA). Norepinephrine (NE) or ANG II with adrenergic (β, α1 and α2) or losartan antagonists was tested for MMP mRNA response in cultured vascular smooth muscle cells (VSMCs). Combined treatment enhances the inhibition of MMP-2 mRNA and protein level induced by simple treatment in AA. However MMP-9 in AA and MMP mRNA in FA were reduced in the same order by treatments. MMP activities were not affected by treatments. The t-PA/PAI-1 ratio, which reflects the fibrinolytic balance, remained higher after treatments. In cultured VSMCs, NE induced stimulation of MMP mRNA via α2 and β adrenergic receptors and MMP-2 activity via β adrenergic receptors, while ANG II-induced stimulation was abrogated by losartan. Overall, there is a synergic inhibition of both systems on the level of MMP-2 in AA.

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