TY - JOUR
T1 - Is osmolality a long-term regulator of renal sympathetic nerve activity in conscious water-deprived rats?
AU - Scrogin, Karie E.
AU - McKeogh, Donogh F.
AU - Brooks, Virginia L.
PY - 2002
Y1 - 2002
N2 - Acute increases in osmolality suppress renal sympathetic nerve activity (RSNA). However, it is not known whether prolonged physiological increases in plasma osmolality chronically inhibit RSNA. To address this hypothesis, mean arterial blood pressure (MAP), heart rate (HR), and RSNA were measured during acute normalization of plasma osmolality in conscious rats made hyperosmotic by 48 h of water deprivation. Water deprivation significantly elevated MAP (120 ± 1 vs. 114 ± 3 mmHg, P < 0.05) and plasma osmolality (306 ± 1 vs. 293 ± 1 mosmol/kgH2O, P < 0.01). When plasma osmolality was subsequently lowered to normal (-17 ± 1 mosmol/kgH2O) with a 2-h (0.12 ml/min) infusion of 5% dextrose in water (5DW), MAP decreased (-11 ± 1 mmHg), and RSNA increased (25 ± 10% baseline). To assess the role of circulating vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist before infusion of 5DW. The antagonist lowered MAP (-4 ± 1 mmHg) and raised RSNA (31 ± 3% baseline) and HR (25 ± 5 beats/min) in water-deprived rats (all changes P < 0.05). However, V1-vasopressin receptor blockade did not increase RSNA or HR independently of baroreflex responses to decreases in arterial pressure. After V1 blockade, infusion of 5DW lowered blood pressure (-8 ± 1 mmHg) but did not further affect HR or RSNA. An isotonic saline infusion that produced the same volume expansion as 5DW lowered MAP (-5 ± 2 mmHg) and HR (-68 ± 2 beats/min) but had no effect on osmolality or RSNA in water-deprived rats. Finally, 5DW infusion had negligible effects in water-replete animals. In conclusion, these results fail to support the hypothesis that sustained increases in plasma osmolality, either directly or via increased vasopressin, tonically suppress RSNA.
AB - Acute increases in osmolality suppress renal sympathetic nerve activity (RSNA). However, it is not known whether prolonged physiological increases in plasma osmolality chronically inhibit RSNA. To address this hypothesis, mean arterial blood pressure (MAP), heart rate (HR), and RSNA were measured during acute normalization of plasma osmolality in conscious rats made hyperosmotic by 48 h of water deprivation. Water deprivation significantly elevated MAP (120 ± 1 vs. 114 ± 3 mmHg, P < 0.05) and plasma osmolality (306 ± 1 vs. 293 ± 1 mosmol/kgH2O, P < 0.01). When plasma osmolality was subsequently lowered to normal (-17 ± 1 mosmol/kgH2O) with a 2-h (0.12 ml/min) infusion of 5% dextrose in water (5DW), MAP decreased (-11 ± 1 mmHg), and RSNA increased (25 ± 10% baseline). To assess the role of circulating vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist before infusion of 5DW. The antagonist lowered MAP (-4 ± 1 mmHg) and raised RSNA (31 ± 3% baseline) and HR (25 ± 5 beats/min) in water-deprived rats (all changes P < 0.05). However, V1-vasopressin receptor blockade did not increase RSNA or HR independently of baroreflex responses to decreases in arterial pressure. After V1 blockade, infusion of 5DW lowered blood pressure (-8 ± 1 mmHg) but did not further affect HR or RSNA. An isotonic saline infusion that produced the same volume expansion as 5DW lowered MAP (-5 ± 2 mmHg) and HR (-68 ± 2 beats/min) but had no effect on osmolality or RSNA in water-deprived rats. Finally, 5DW infusion had negligible effects in water-replete animals. In conclusion, these results fail to support the hypothesis that sustained increases in plasma osmolality, either directly or via increased vasopressin, tonically suppress RSNA.
KW - Arterial pressure
KW - Heart rate
KW - RSNA
KW - Vasopressin
KW - Water deprivation
UR - http://www.scopus.com/inward/record.url?scp=0036088256&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036088256&partnerID=8YFLogxK
U2 - 10.1152/ajpregu.00780.2000
DO - 10.1152/ajpregu.00780.2000
M3 - Article
C2 - 11792667
AN - SCOPUS:0036088256
SN - 0363-6119
VL - 282
SP - R560-R568
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 2 51-2
ER -