Osmolality: A physiological long-term regulator of lumbar sympathetic nerve activity and arterial pressure

Karie E. Scrogin, Eugene T. Grygielko, Virginia Brooks

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Abstract

Acute infusion of hypertonic fluid increases mean arterial pressure (MAP) in part by elevating nonrenal sympathetic activity. However, it is not known whether chronic, physiological increases in osmolality also increase sympathetic activity. To test this hypothesis, MAP, heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured in conscious, 48-h water-deprived rats (WD) during a progressive reduction in osmolality produced by a 2-h systemic infusion (0.12 ml/min) of 5% dextrose in water (5DW). Water deprivation significantly increased osmolality (308 ± 2 vs. 290 ± 2 mosmol/kgH2O, P <0.001), HR (453 ± 7 vs. 421 ± 10 beats/min, P <0.05), and LSNA (63.5 ± 1.8 vs. 51.9 ± 3.8% baroreflex maximum, P <0.01). Two hours of 5DW infusion reduced osmolality (-15 ± 5 mosmol/kgH2O), LSNA (-23 ± 3% baseline), and MAP (-10 ± 1 mmHg). To evaluate the role of vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist. The antagonist lowered MAP (-5 ± 1 mmHg) and elevated HR (32 ± 7 beats/min) and LSNA (11 ± 3% baseline) in WD (P <0.05), but not in water-replete, rats. 5DW infusion had a similar cumulative effect on all variables in V1-blocked WD rats, but had no effect in water-replete rats. Infusion of the same volume of normal saline in WD rats did not change osmolality, LSNA or MAP. Together these data indicate that, in dehydrated rats, vasopressin supports MAP and suppresses LSNA and HR and that physiological changes in osmolality directly influence sympathetic activity and blood pressure independently of changes in vasopressin and blood volume.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume276
Issue number6 45-6
StatePublished - Jun 1999

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

Keywords

  • Conscious rats
  • Heart rate
  • Sodium chloride
  • V-vasopressin antagonist
  • Vasopressin

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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title = "Osmolality: A physiological long-term regulator of lumbar sympathetic nerve activity and arterial pressure",
abstract = "Acute infusion of hypertonic fluid increases mean arterial pressure (MAP) in part by elevating nonrenal sympathetic activity. However, it is not known whether chronic, physiological increases in osmolality also increase sympathetic activity. To test this hypothesis, MAP, heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured in conscious, 48-h water-deprived rats (WD) during a progressive reduction in osmolality produced by a 2-h systemic infusion (0.12 ml/min) of 5{\%} dextrose in water (5DW). Water deprivation significantly increased osmolality (308 ± 2 vs. 290 ± 2 mosmol/kgH2O, P <0.001), HR (453 ± 7 vs. 421 ± 10 beats/min, P <0.05), and LSNA (63.5 ± 1.8 vs. 51.9 ± 3.8{\%} baroreflex maximum, P <0.01). Two hours of 5DW infusion reduced osmolality (-15 ± 5 mosmol/kgH2O), LSNA (-23 ± 3{\%} baseline), and MAP (-10 ± 1 mmHg). To evaluate the role of vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist. The antagonist lowered MAP (-5 ± 1 mmHg) and elevated HR (32 ± 7 beats/min) and LSNA (11 ± 3{\%} baseline) in WD (P <0.05), but not in water-replete, rats. 5DW infusion had a similar cumulative effect on all variables in V1-blocked WD rats, but had no effect in water-replete rats. Infusion of the same volume of normal saline in WD rats did not change osmolality, LSNA or MAP. Together these data indicate that, in dehydrated rats, vasopressin supports MAP and suppresses LSNA and HR and that physiological changes in osmolality directly influence sympathetic activity and blood pressure independently of changes in vasopressin and blood volume.",
keywords = "Conscious rats, Heart rate, Sodium chloride, V-vasopressin antagonist, Vasopressin",
author = "Scrogin, {Karie E.} and Grygielko, {Eugene T.} and Virginia Brooks",
year = "1999",
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language = "English (US)",
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journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
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TY - JOUR

T1 - Osmolality

T2 - A physiological long-term regulator of lumbar sympathetic nerve activity and arterial pressure

AU - Scrogin, Karie E.

AU - Grygielko, Eugene T.

AU - Brooks, Virginia

PY - 1999/6

Y1 - 1999/6

N2 - Acute infusion of hypertonic fluid increases mean arterial pressure (MAP) in part by elevating nonrenal sympathetic activity. However, it is not known whether chronic, physiological increases in osmolality also increase sympathetic activity. To test this hypothesis, MAP, heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured in conscious, 48-h water-deprived rats (WD) during a progressive reduction in osmolality produced by a 2-h systemic infusion (0.12 ml/min) of 5% dextrose in water (5DW). Water deprivation significantly increased osmolality (308 ± 2 vs. 290 ± 2 mosmol/kgH2O, P <0.001), HR (453 ± 7 vs. 421 ± 10 beats/min, P <0.05), and LSNA (63.5 ± 1.8 vs. 51.9 ± 3.8% baroreflex maximum, P <0.01). Two hours of 5DW infusion reduced osmolality (-15 ± 5 mosmol/kgH2O), LSNA (-23 ± 3% baseline), and MAP (-10 ± 1 mmHg). To evaluate the role of vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist. The antagonist lowered MAP (-5 ± 1 mmHg) and elevated HR (32 ± 7 beats/min) and LSNA (11 ± 3% baseline) in WD (P <0.05), but not in water-replete, rats. 5DW infusion had a similar cumulative effect on all variables in V1-blocked WD rats, but had no effect in water-replete rats. Infusion of the same volume of normal saline in WD rats did not change osmolality, LSNA or MAP. Together these data indicate that, in dehydrated rats, vasopressin supports MAP and suppresses LSNA and HR and that physiological changes in osmolality directly influence sympathetic activity and blood pressure independently of changes in vasopressin and blood volume.

AB - Acute infusion of hypertonic fluid increases mean arterial pressure (MAP) in part by elevating nonrenal sympathetic activity. However, it is not known whether chronic, physiological increases in osmolality also increase sympathetic activity. To test this hypothesis, MAP, heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured in conscious, 48-h water-deprived rats (WD) during a progressive reduction in osmolality produced by a 2-h systemic infusion (0.12 ml/min) of 5% dextrose in water (5DW). Water deprivation significantly increased osmolality (308 ± 2 vs. 290 ± 2 mosmol/kgH2O, P <0.001), HR (453 ± 7 vs. 421 ± 10 beats/min, P <0.05), and LSNA (63.5 ± 1.8 vs. 51.9 ± 3.8% baroreflex maximum, P <0.01). Two hours of 5DW infusion reduced osmolality (-15 ± 5 mosmol/kgH2O), LSNA (-23 ± 3% baseline), and MAP (-10 ± 1 mmHg). To evaluate the role of vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist. The antagonist lowered MAP (-5 ± 1 mmHg) and elevated HR (32 ± 7 beats/min) and LSNA (11 ± 3% baseline) in WD (P <0.05), but not in water-replete, rats. 5DW infusion had a similar cumulative effect on all variables in V1-blocked WD rats, but had no effect in water-replete rats. Infusion of the same volume of normal saline in WD rats did not change osmolality, LSNA or MAP. Together these data indicate that, in dehydrated rats, vasopressin supports MAP and suppresses LSNA and HR and that physiological changes in osmolality directly influence sympathetic activity and blood pressure independently of changes in vasopressin and blood volume.

KW - Conscious rats

KW - Heart rate

KW - Sodium chloride

KW - V-vasopressin antagonist

KW - Vasopressin

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