Effect of muscimol and l-NAME in the PVN on the RSNA response to volume expansion in conscious rabbits

2004 ◽  
Vol 287 (4) ◽  
pp. F739-F746 ◽  
Author(s):  
Chi Wai Ng ◽  
Robert De Matteo ◽  
Emilio Badoer
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Neuronal Function ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Dextran 70 ◽  
Oxide Synthase ◽  
Renal Sympathetic

In the present study, we have investigated whether the hypothalamic paraventricular nucleus (PVN) contributed to the reflex reduction in renal sympathetic nerve activity (RSNA) normally elicited by volume expansion in the conscious rabbit. RSNA was monitored after volume expansion (Dextran 70, 2 ml/min for 30 min) in animals microinjected into, and outside, the PVN with muscimol (10 nmol), to acutely inhibit neuronal function. Because nitric oxide within the PVN inhibits RSNA, we also examined the effect of NG-nitro-l-arginine methyl ester (l-NAME; 20 nmol) to block nitric oxide synthase. Compared with vehicle, the reduction in RSNA elicited by volume expansion was abolished by injection of muscimol into the PVN. The effect was specific to the PVN because microinjections of muscimol outside the PVN had no effect on the response. l-NAME microinjected into or outside the PVN had no effect on the RSNA response. The findings suggest that the PVN is essential in the central pathways mediating the renal sympathetic nerve response elicited by elevations in plasma volume but that nitric oxide does not play a major role.

Role of nitric oxide in regulation of renal sympathetic nerve activity during hemorrhage in conscious rats

1999 ◽  
Vol 277 (1) ◽  
pp. H8-H14 ◽  
Author(s):  
Yoshihide Fujisawa ◽  
Naoko Mori ◽  
Kouichi Yube ◽  
Hiroshi Miyanaka ◽  
Akira Miyatake ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Saline Group ◽  
Baroreceptor Reflex ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rats ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The effect of inhibition of nitric oxide (NO) synthesis on the responses of blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) during hemorrhaging was examined with the use of an NO synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), in conscious rats. In the 0.9% saline group, hemorrhage (10 ml/kg body wt) did not alter BP but significantly increased HR and RSNA by 88 ± 12 beats/min and 67 ± 12%, respectively. Intravenous infusion of l-NAME (50 μg ⋅ kg−1⋅ min−1) significantly attenuated these tachycardic and sympathoexcitatory responses to hemorrhage (14 ± 7 beats/min and 26 ± 12%, respectively). Pretreatment ofl-arginine (87 mg/kg) recovered the attenuation of HR and RSNA responses induced byl-NAME (92 ± 6 beats/min and 64 ± 10%, respectively).l-NAME by itself did not alter the baroreceptor reflex control of HR and RSNA. Hemorrhage increased the plasma vasopressin concentration, and its increment in thel-NAME-treated group was significantly higher than that in the 0.9% saline group. Pretreatment with the vascular arginine vasopressin V1-receptor antagonist OPC-21268 (5 mg/kg) recovered the attenuation of RSNA response induced byl-NAME (54 ± 7%). These results indicate that NO modulated HR and RSNA responses to hemorrhage but did not directly affect the baroreceptor reflex arch. It can be assumed that NO modulated the baroreflex function by altering the secretion of vasopressin induced by hemorrhage.

Cardiac afferents play the dominant role in renal nerve inhibition elicited by volume expansion in the rabbit

1998 ◽  
Vol 274 (2) ◽  
pp. R383-R388 ◽  
Author(s):  
Emilio Badoer ◽  
Viatcheslav Moguilevski ◽  
Barry P. McGrath
Keyword(s):  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Dominant Role ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Conscious Rabbit ◽  
Renal Sympathetic Nerve ◽  
Cardiac Afferents ◽  
Renal Sympathetic

In the rabbit, vagotomy combined with arterial baroreceptor denervation abolishes the renal sympathoinhibition elicited by volume expansion. However, the effect of removing cardiopulmonary afferents alone has not been investigated. The aim of the present study was to determine the role of the cardiac afferents in the renal sympathetic response elicited by volume expansion in the normal conscious rabbit. Four experimental groups were used in which rabbits were administered 1) volume expansion (Haemaccel, 1.9 ml/min for 60 min), 2) volume expansion + bolus intrapericardial procaine (20 mg) to block cardiac afferents, 3) volume expansion + intravenous procaine (20 mg bolus), and 4) intrapericardial procaine alone (20 mg bolus). Volume expansion did not significantly affect mean arterial pressure or heart rate but produced a profound fall in renal sympathetic nerve activity (∼50%). Intrapericardial procaine administered 30 min after the start of volume expansion markedly reversed the renal sympathoinhibition to within 20% of the pre-volume expansion level, an effect that wore off over 25 min. In contrast, intravenous procaine lowered renal sympathetic nerve activity slightly further. The results suggest that cardiac afferents play the dominant role in the renal sympathoinhibition in response to volume expansion in the normal conscious rabbit.

Effects of volume expansion on renal sympathetic nerve activity and cardiovascular and renal function in lambs

1992 ◽  
Vol 262 (4) ◽  
pp. R651-R658 ◽  
Author(s):  
F. G. Smith ◽  
J. M. Klinkefus ◽  
J. E. Robillard
Keyword(s):  
Renal Function ◽  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Right Atrial ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Cardiopulmonary Baroreflex ◽  
Renal Sympathetic

To assess the cardiopulmonary baroreflex in the immature animal, effects of volume expansion on changes in right atrial pressure, renal sympathetic nerve activity, and renal function were measured in chronically instrumented newborn (4-8 days; n = 13) and older lambs (4-5 wk; n = 14). Studies were carried out for 30 min before and 2 h after volume expansion with 6% Dextran 70 (25 ml/kg). Right atrial pressure increased by 4.0 +/- 0.5 mmHg in newborns and by 8.8 +/- 0.6 mmHg in older lambs within 15 min of volume expansion (P less than 0.001). After volume expansion, heart rate decreased in newborns from 237 +/- 6 beats/min to a nadir of 211 +/- 7 beats/min 2 h later (P less than 0.001) but remained constant at control levels of 148 +/- 9 beats/min in older lambs. Maximal inhibition of renal sympathetic nerve activity was achieved at 15 min in older lambs (-50.1 +/- 7.5%) and at 60 min (-58.3 +/- 10.9%) in newborns in which there was a prolonged sympathoinhibition (P less than 0.001). There was also a significant diuretic response in both groups but a limited natriuretic response to volume expansion in newborns (P greater than 0.05) compared with older lambs (P less than 0.001). These data demonstrate the presence of the cardiopulmonary baroreflex in the first week of life in lambs. The sustained sympathoinhibition and bradycardia seen in response to volume expansion in newborns but not in older lambs support the hypothesis that the reflexes controlling arterial pressure and blood volume change with postnatal maturation.

High-NaCl diet reduces cardiac vagal afferent nerve response to volume expansion

1987 ◽  
Vol 252 (4) ◽  
pp. R687-R692
Author(s):  
G. F. Dibona ◽  
L. L. Sawin
Keyword(s):  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Afferent Nerve ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Vagal Afferent ◽  
Renal Sympathetic

To localize the mechanism by which high dietary NaCl intake decreases the reflex inhibitory effects of intravenous volume expansion on efferent renal sympathetic nerve activity, experiments were performed in anesthetized normal rats prepared for separate examination of the afferent and efferent limbs of the cardiopulmonary baroreceptor reflex. When left ventricular end-diastolic pressure, an index of left heart filling pressure, was progressively increased by intravenous isotonic saline administration in sinoaortic-denervated rats, the increase in cardiac vagal afferent nerve activity was less in rats consuming high compared with normal dietary NaCl intake. During electrical stimulation of the central vagus nerve in sinoaortic-denervated rats, the decreases in efferent renal sympathetic nerve activity were similar in rats consuming high and normal dietary NaCl intake. Thus the effect of high dietary NaCl intake to decrease overall cardiopulmonary baroreceptor reflex gain during intravenous volume expansion is located in the afferent limb of the reflex arc.

Role of renal sympathetic nerve activity in hypertension induced by chronic nitric oxide inhibition

2007 ◽  
Vol 292 (4) ◽  
pp. R1479-R1485 ◽  
Author(s):  
Rohit Ramchandra ◽  
Carolyn J. Barrett ◽  
Sarah-Jane Guild ◽  
Fiona McBryde ◽  
Simon C. Malpas
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Baseline Levels ◽  
Renal Sympathetic

Nitric oxide levels are diminished in hypertensive patients, suggesting nitric oxide might have an important role to play in the development of hypertension. Chronic blockade of nitric oxide leads to hypertension that is sustained throughout the period of the blockade in baroreceptor-intact animals. It has been suggested that the sympathetic nervous system is involved in the chronic increase in blood pressure; however, the evidence is inconclusive. We measured renal sympathetic nerve activity and blood pressure via telemetry in rabbits over 7 days of nitric oxide blockade. Nitric oxide blockade via Nω-nitro-l-arginine methyl ester (l-NAME) in the drinking water (50 mg·kg−1·day−1) for 7 days caused a significant increase in arterial pressure (7 ± 1 mmHg above control levels; P < 0.05). While the increase in blood pressure was associated with a decrease in heart rate (from 233 ± 6 beats/min before the l-NAME to 202 ± 6 beats/min on day 7), there was no change in renal sympathetic nerve activity (94 ± 4 %baseline levels on day 2 and 96 ± 5 %baseline levels on day 7 of l-NAME; baseline nerve activity levels were normalized to the maximum 2 s of nerve activity evoked by nasopharyngeal stimulation). The lack of change in renal sympathetic nerve activity during the l-NAME-induced hypertension indicates that the renal nerves do not mediate the increase in blood pressure in conscious rabbits.

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