Is osmolality a long-term regulator of renal sympathetic nerve activity in conscious water-deprived rats?

Karie E. Scrogin, Donogh F. McKeogh, Virginia Brooks

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23 Citations (Scopus)

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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume282
Issue number2 51-2
StatePublished - 2002

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Osmolar Concentration
Arterial Pressure
Kidney
Water
Vasopressin Receptors
Heart Rate
Glucose
Water Deprivation
Vasopressins
Baroreflex
Blood Pressure

Keywords

  • Arterial pressure
  • Heart rate
  • RSNA
  • Vasopressin
  • Water deprivation

ASJC Scopus subject areas

  • Physiology

Cite this

@article{252990a58304418283b9113fd6b039c0,
title = "Is osmolality a long-term regulator of renal sympathetic nerve activity in conscious water-deprived rats?",
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.",
keywords = "Arterial pressure, Heart rate, RSNA, Vasopressin, Water deprivation",
author = "Scrogin, {Karie E.} and McKeogh, {Donogh F.} and Virginia Brooks",
year = "2002",
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volume = "282",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "2 51-2",

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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

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

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