Tags

Type your tag names separated by a space and hit enter

Is osmolality a long-term regulator of renal sympathetic nerve activity in conscious water-deprived rats?
Am J Physiol Regul Integr Comp Physiol. 2002 Feb; 282(2):R560-8.AJ

Abstract

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.

Authors+Show Affiliations

Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, Oregon 97201, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11792667

Citation

Scrogin, Karie E., et al. "Is Osmolality a Long-term Regulator of Renal Sympathetic Nerve Activity in Conscious Water-deprived Rats?" American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, vol. 282, no. 2, 2002, pp. R560-8.
Scrogin KE, McKeogh DF, Brooks VL. Is osmolality a long-term regulator of renal sympathetic nerve activity in conscious water-deprived rats? Am J Physiol Regul Integr Comp Physiol. 2002;282(2):R560-8.
Scrogin, K. E., McKeogh, D. F., & Brooks, V. L. (2002). Is osmolality a long-term regulator of renal sympathetic nerve activity in conscious water-deprived rats? American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 282(2), R560-8.
Scrogin KE, McKeogh DF, Brooks VL. Is Osmolality a Long-term Regulator of Renal Sympathetic Nerve Activity in Conscious Water-deprived Rats. Am J Physiol Regul Integr Comp Physiol. 2002;282(2):R560-8. PubMed PMID: 11792667.
* Article titles in AMA citation format should be in sentence-case
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 - 2002/1/17/pubmed PY - 2002/2/15/medline PY - 2002/1/17/entrez SP - R560 EP - 8 JF - American journal of physiology. Regulatory, integrative and comparative physiology JO - Am. J. Physiol. Regul. Integr. Comp. Physiol. VL - 282 IS - 2 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. SN - 0363-6119 UR - https://www.unboundmedicine.com/medline/citation/11792667/Is_osmolality_a_long_term_regulator_of_renal_sympathetic_nerve_activity_in_conscious_water_deprived_rats L2 - http://www.physiology.org/doi/full/10.1152/ajpregu.00780.2000?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -