Regulation of drinking and vasopressin secretion: role of organum vasculosum laminae terminalis

1987 ◽  
Vol 253 (1) ◽  
pp. R108-R120 ◽  
Author(s):  
T. N. Thrasher ◽  
L. C. Keil
Keyword(s):  
Conscious Dogs ◽  
Ang Ii ◽  
Cellular Dehydration ◽  
Organum Vasculosum Laminae Terminalis ◽  
Before And After ◽  
Electrolytic Ablation ◽  
Vasopressin Secretion ◽  
Osmotic Stimulus ◽  
Organum Vasculosum

We have proposed that the organum vasculosum laminae terminalis (OVLT) contains osmoreceptors involved in the regulation of drinking and secretion of arginine vasopressin (AVP) in the dog. By use of the technique of electrolytic ablation, conscious dogs were evaluated for their responses to acute peripheral challenges of hypertonic NaCl and angiotensin II (ANG II) and hemorrhage (20 ml/kg) before and after destruction of the OVLT (n = 7) or adjacent tissue (n = 9) as a control. Lesions confined to the tip of the optic recess and destroying greater than 90% of the OVLT caused a dramatic increase in the threshold to drink and increase plasma AVP levels and a significant (P less than 0.01) reduction in the magnitude of these responses to an osmotic stimulus. Drinking and secretion of AVP in response to ANG II, but not the rise in peripheral corticosteroids, were also blocked (P less than 0.01) by ablation of the OVLT. In contrast responses to hemorrhage were not affected by the lesion. These results support the hypothesis that the OVLT contains osmoreceptors involved in physiological responses to cellular dehydration and suggest involvement in drinking and secretion of AVP in response to ANG II. The results also indicate that forebrain mechanisms which depend on the OVLT are independent of mechanisms responding to hemorrhage in conscious dogs.

Increased alpha 1-adrenergic vascular sensitivity during development of hypertension in conscious dogs

1993 ◽  
Vol 264 (4) ◽  
pp. H1259-H1268 ◽  
Author(s):  
N. Uemura ◽  
D. E. Vatner ◽  
Y. T. Shen ◽  
J. Wang ◽  
S. F. Vatner
Keyword(s):  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Conscious Dogs ◽  
Aortic Tissue ◽  
Ang Ii ◽  
Receptor Density ◽  
Adrenergic Stimulation ◽  
Before And After ◽  
Vascular Responsiveness

The goal of this study was to determine whether enhanced vascular responsiveness during the development of perinephritic hypertension is selective or nonspecific. The effects of graded infusions of norepinephrine (NE), phenylephrine (PE), angiotensin II (ANG II), and vasopressin (VP) were examined on mean arterial pressure, total peripheral resistance (TPR), and aortic pressure-diameter relationships in conscious dogs. NE increased TPR significantly greater (P < 0.01) in hypertension than normotension, as did PE infusion, whereas ANG II and VP increased TPR similarly before and after hypertension. Analysis of aortic pressure-diameter relationships also demonstrated significant (P < 0.05) shifts in response to NE and PE, but not ANG II and VP, during the development of hypertension. In normotensive dogs, low doses of ANG II infusion also enhanced the vasoconstrictor response not only to NE and PE but also to VP. In contrast to what was observed in hypertension, in the presence of ANG II infusion after ganglionic blockade, enhanced responses to PE and NE were no longer observed. The alpha 1-adrenergic receptor density in membrane preparations from aortic tissue, as determined by [3H]prazosin binding, was higher (P < 0.05) in hypertensive dogs than control dogs. Thus the vascular responsiveness in the aorta and resistance vessels is enhanced to alpha 1-adrenergic stimulation, but not to all vasoconstrictors, during developing perinephritic hypertension. The mechanism appears to involve increased alpha 1-adrenergic receptor density.

Role of the descending pressor pathway in the conscious and pentobarbital-anesthetized dog

1978 ◽  
Vol 234 (2) ◽  
pp. H152-H156
Author(s):  
G. S. Geis ◽  
G. Barratt ◽  
R. D. Wurster
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Control ◽  
Conscious Dogs ◽  
Cardiovascular Parameters ◽  
Bilateral Carotid ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Conscious Animals

Resting cardiovascular parameters and the responses to bilateral carotid occlusions (BCO) were monitored in pentobarbital-anesthetized and conscious dogs before and after placing lesions in the dorsolateral funiculi at C7-C8 and after spinal transections at C7. Pre- and postlesion blood pressure (BP) and heart rate (HR) responses to exercise were also monitored. The lesions significantly attenuated the responses to BCO and decreased resting BP in anesthetized dogs. Yet neither resting HR in anesthetized or conscious dogs nor the resting BP in conscious dogs was affected by the lesions. Subsequent spinal transections significantly decreased resting HR and BP and the responses to BCO but did not affect the BP response to BCO in anesthetized dogs as compared with corresponding postlesion parameters. BP responses to exercise were significantly attenuated by the lesions, but HR responses were not affected. Since stimulation and BP studies indicated that the descending pressor pathway had been ablated, the data suggest that the pathway mediates BP and HR responses to BCO in pentobarbital-anesthetized and conscious dogs. It does not maintain resting HR in anesthetized or conscious animals, and the resting BP in conscious dogs. This pathway is important for BP responses to exercise but is not necessary for HR responses. Finally, other spinal pathways are involved in cardiovascular control.

Effect of renal denervation on the suppression of renin secretion by vasopressin in conscious dogs

1984 ◽  
Vol 247 (6) ◽  
pp. F881-F887 ◽  
Author(s):  
L. C. Gregory ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Conscious Dogs ◽  
Reflex Response ◽  
Renal Nerves ◽  
Ang Ii ◽  
Before And After

Previous studies have shown that the inhibition of renin secretion by vasopressin (AVP) in conscious dogs is related to vasoconstrictor activity and may be a reflex response mediated by the renal nerves. The aim of the present experiments was to determine whether the suppression of plasma renin activity (PRA) by AVP is blocked by renal denervation. AVP and, for comparison, angiotensin II (ANG II) were infused intravenously for 45 min in seven conscious dogs before and after bilateral renal denervation. Before denervation, AVP infusion at 0.2 and 1.0 ng X kg-1 X min-1 suppressed PRA from 7.4 +/- 1.1 to 4.7 +/- 1.0 (P less than 0.01) and from 7.9 +/- 1.8 to 3.8 +/- 0.8 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. ANG II infusion at 5.0 and 10.0 ng X kg-1 X min-1 decreased PRA from 7.5 +/- 2.3 to 2.5 +/- 0.7 (P less than 0.01) and from 6.0 +/- 1.1 to 1.8 +/- 0.4 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. One to three weeks following renal denervation, PRA had decreased from 6.7 +/- 1.3 to 2.9 +/- 0.5 ng X ml-1 X 3 h-1 (P less than 0.01), and renal norepinephrine was undetectable. After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the organum vasculosum laminae terminalis in the control of gonadotrophin secretion in rats

1982 ◽  
Vol 93 (3) ◽  
pp. 355-NP ◽  
Author(s):  
F. Piva ◽  
P. Limonta ◽  
L. Martini
Keyword(s):  
Ovariectomized Rats ◽  
Adult Rats ◽  
Organum Vasculosum Laminae Terminalis ◽  
Serum Lh ◽  
Parallel Increase ◽  
Gonadotrophin Secretion ◽  
Radiofrequency Lesions ◽  
Organum Vasculosum

The organum vasculosum laminae terminalis (OVLT) was destroyed by radiofrequency lesions in regularly cycling and in long-term ovariectomized adult rats. After OVLT lesion practically all cyclic females (16 out of 22) became dioestrous, as indicated by vaginal smears. At the time of killing these animals (8 days after the lesion) serum LH levels were undetectable, while serum FSH was as low as in cyclic animals in dioestrus. In the few OVLT-lesioned animals which exhibited some sort of oestrous cyclicity, serum LH showed a small subphysiological increase at pro-oestrus: this was not accompanied by a parallel increase in serum FSH and in these animals a delayed peak of FSH occurred on the day of oestrus. Ovariectomized rats bearing OVLT lesions had serum titres of LH and FSH as high as those of ovariectomized control rats. It is suggested that the OVLT may play a role in the control of the cyclic release of gonadotrophins but is not involved in the tonic regulation of gonadotrophin secretion.

Enhanced left ventricular shortening during chronic volume overload in conscious dogs

1980 ◽  
Vol 238 (2) ◽  
pp. H126-H133 ◽  
Author(s):  
M. M. LeWinter ◽  
R. L. Engler ◽  
J. S. Karliner
Keyword(s):  
Volume Overload ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Stimulation ◽  
Ventricular Performance ◽  
Blood Pressure Elevation ◽  
Chronic Volume Overload ◽  
Before And After ◽  
Ejection Phase

Prior work with the arteriovenous fistula model indicates that left ventricular performance is at least normal and may be enhanced during chronic volume overload. The present study was undertaken in conscious dogs to determine whether ejection-phase indices of ventricular function are enhanced after 1 mo of volume overload, using an experimental design in which loading conditions could be accounted for and animals were used as their own controls before and after volume overload. We also examined the response of the volume-overloaded left ventricle to an afterload stress and the role of adrenergic stimulation in maintenance of function. Both at rest and during hemodynamically matched conditions, percent shortening (ultrasonic dimension gauges) and mean shortening rates were increased during volume overload. This difference was maintained during phenylephrine-induced blood pressure elevation, although diastolic dimensions increased more in control studies during phenylephrine. Propranolol produced significantly larger reductions in these indices during volume overload than in the control state. Thus, ejection-phase function is enhanced during volume overload, at least in part due to increased adrenergic stimulation.

Effect of PTH on blood pressure and response to vasoconstrictor agonists

1985 ◽  
Vol 248 (5) ◽  
pp. F674-F681 ◽  
Author(s):  
Y. Saglikes ◽  
S. G. Massry ◽  
K. Iseki ◽  
J. L. Nadler ◽  
V. M. Campese
Keyword(s):  
Blood Pressure ◽  
Inhibitory Effect ◽  
Significant Rise ◽  
Ang Ii ◽  
Vascular Response ◽  
Hypotensive Action ◽  
Amino Terminal ◽  
Before And After ◽  
Hypotensive Response

Parathyroid hormone (PTH) is known to be a vasodilator and to exert a hypotensive action. The present study examined the possible mechanisms involved, with special emphasis on the role of vasodilatory prostaglandins. The effects of the intact 1-84 PTH and that of its amino-terminal 1-34 fragment on mean arterial pressure (MAP) and on the vascular response to norepinephrine (NE) or angiotensin II (ANG II) were examined in rats before and after pretreatment with indomethacin. Bolus injections of 30 U of both 1-84 and 1-34 PTH produced a significant (P less than 0.01) decrease in MAP; however, the hypotensive response to 1-34 PTH (-28 +/- 4.6 mmHg) was more marked (P less than 0.01) than to 1-84 PTH (-9 +/- 1.8 mmHg). The infusion of 1-84 PTH (30 U/h) did not alter MAP, whereas the infusion of 1-34 PTH (30 U/h) led to a decrease in MAP from 124 +/- 2 to 103 +/- 4.0 mmHg (P less than 0.01) and to a rise in heart rate from 359 +/- 30 to 437 +/- 13 beats/min (P less than 0.02). Both 1-84 and 1-34 PTH antagonized the pressor effects produced by bolus injections of NE and ANG II. Pretreatment with indomethacin (5 mg/kg body wt) abolished the inhibitory effect of 1-84 and 1-34 PTH on the response of MAP to NE and ANG II and the hypotensive action of 1-34 PTH. Infusion of 1-84 and 1-34 PTH produced a significant rise in urinary excretion of 6-keto-PGF1 alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of endogenous angiotensin II on sympathetic reflexes in conscious rabbits

1997 ◽  
Vol 272 (6) ◽  
pp. R1816-R1825 ◽  
Author(s):  
R. D. Bendle ◽  
S. C. Malpas ◽  
G. A. Head
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Ang Ii ◽  
At1 Antagonist ◽  
Before And After ◽  
Sympathetic Reflexes ◽  
Conscious Rabbits ◽  
Dose Dependent ◽  
Renal Sympathetic

In the present study we sought to determine the contribution of endogenous brain stem angiotensin to renal sympathetic reflexes in conscious rabbits. Initial studies determined the subtype of receptor involved in the pressor response to angiotensin II (ANG II) administration into the fourth ventricle (4V). The AT1 antagonist losartan (0.001-10 micrograms 4V) had no effect on blood pressure alone but caused a dose-dependent blockade of the pressor effect of ANG II, with complete blockade produced by 10 micrograms, an effect that lasted for at least 3 h. The AT2 antagonist PD-123319 (0.1-1,000 micrograms) and vehicle had no effect on the ANG II pressor response. The effect of losartan (10 micrograms) on the baroreceptor, chemoreceptor, and trigeminal reflexes was examined in eight rabbits that had been implanted with 4V catheters and an electrode for recording renal sympathetic nerve activity (RSNA) 1 wk earlier. Baroreflex assessments were made during normoxia and two conditions of hypoxia (10% O2 and 10% O2 + 3% CO2) before and after 10 micrograms losartan or vehicle, on separate experimental days. During normoxia and hypoxia+CO2 losartan increased resting RSNA, the range, and upper plateau of the RSNA-MAP baroreflex curves. By contrast the marked increase in RSNA due to activation of trigeminal afferents was not affected by losartan. In conclusion the effect of losartan to increase RSNA activity in conscious rabbits, particularly during hypoxia and baroreceptor unloading, suggests that endogenous ANG II via AT1 receptors normally inhibits renal sympathetic baroreceptor and chemoreceptor reflexes.

AT1 receptors in the nucleus tractus solitarii mediate the interaction between the baroreflex and the cardiac sympathetic afferent reflex in anesthetized rats

2007 ◽  
Vol 292 (3) ◽  
pp. R1137-R1145 ◽  
Author(s):  
Wei-Zhong Wang ◽  
Lie Gao ◽  
Yan-Xia Pan ◽  
Irving H. Zucker ◽  
Wei Wang
Keyword(s):  
Extracellular Recording ◽  
Nucleus Tractus Solitarii ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Anesthetized Rats ◽  
Before And After ◽  
Cardiac Sympathetic Afferent Reflex ◽  
Induced Changes

The cardiac “sympathetic afferent” reflex (CSAR) has been reported to increase sympathetic outflow and depress baroreflex function via a central angiotensin II (ANG II) mechanism. In the present study, we examined the role of ANG II type 1 (AT1) receptors in the nucleus tractus solitarii (NTS) in mediating the interaction between the CSAR and the baroreflex in anesthetized rats. We examined the effects of bilateral microinjection of AT1 receptor antagonist losartan (100 pmol) into the NTS on baroreflex control of renal sympathetic nerve activity (RSNA) before and after CSAR activation by epicardial application of capsaicin (0.4 μg). Using single-unit extracellular recording, we further examined the effects of CSAR activation on the barosensitivity of barosensitive NTS neurons and the effects of intravenous losartan (2 mg/kg) on CSAR-induced changes in activity of NTS barosensitive neurons. Bilateral NTS microinjection of losartan significantly attenuated the increases in arterial pressure, heart rate, and RSNA evoked by capsaicin but also markedly ( P < 0.01) reversed the CSAR-induced blunted baroreflex control of RSNA (Gainmax from 1.65 ± 0.10 to 2.22 ± 0.11%/mmHg). In 17 of 24 (70.8%) NTS barosensitive neurons, CSAR activation significantly ( P < 0.01) inhibited the baseline neuronal activity and attenuated the neuronal barosensitivity. In 11 NTS barosensitive neurons, intravenous losartan effectively ( P < 0.01) normalized the decreased neuronal barosensitivity induced by CSAR activation. In conclusion, blockade of NTS AT1 receptors improved the blunted baroreflex during CSAR activation, suggesting that the NTS plays an important role in processing the interaction between the baroreflex and the CSAR via an AT1 receptor-dependent mechanism.

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