Sympathetic augmentation of cardiac function in developing hypertension in conscious dogs

R. J. Gelpi, L. Hittinger, A. M. Fujii, V. M. Crocker, I. Mirsky, Stephen Vatner

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

To determine the alterations in left ventricular (LV) function and the mechanisms involved that occur during the development of perinephritic hypertension, dogs were instrumented with a miniature LV pressure transducer, aortic and left atrial catheters, and ultrasonic crystals to measure LV diameter in the short and long axes and wall thickness. At 2 wk after initiation of perinephritic hypertension, increases (P < 0.05) were observed in LV systolic pressure, LV end-diastolic pressure, both short- and long-axis end-diastolic diameters, calculated LV end-diastolic volume, stroke volume, global average LV systolic wall stress, first derivative of LV pressure (LV dP/dt), and ejection fraction, whereas mean velocity of circumferential fiber shortening (V(cf)) and rate of change of VL short-axis diameter (LV dD/dt) rose but not significantly. At three levels of matched preload and afterload induced by the administration of graded doses of phenylephrine, V(cf), LV dD/dt, and LV dP/dt increased in hypertension compared with the same levels of preload and afterload before hypertension. When the loading conditions in the normotensive and hypertensive dogs were matched, either after ganglionic blockade or β-adrenergic blockade, both isovolumic and ejection-phase indexes of LV function remained similar before and after hypertension. Thus we conclude that 1) LV function in intact, conscious dogs with early hypertension is enhanced, and 2) the major mechanism for the increase in LV function involves the sympathetic nervous system.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume255
Issue number6
StatePublished - Dec 1 1988

Fingerprint

Dogs
Hypertension
Left Ventricular Function
Ventricular Pressure
Stroke Volume
Blood Pressure
Pressure Transducers
Sympathetic Nervous System
Phenylephrine
Ultrasonics
Adrenergic Agents
Catheters

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

@article{3bdfc87f2d484b138f435690e35c5f9a,
title = "Sympathetic augmentation of cardiac function in developing hypertension in conscious dogs",
abstract = "To determine the alterations in left ventricular (LV) function and the mechanisms involved that occur during the development of perinephritic hypertension, dogs were instrumented with a miniature LV pressure transducer, aortic and left atrial catheters, and ultrasonic crystals to measure LV diameter in the short and long axes and wall thickness. At 2 wk after initiation of perinephritic hypertension, increases (P < 0.05) were observed in LV systolic pressure, LV end-diastolic pressure, both short- and long-axis end-diastolic diameters, calculated LV end-diastolic volume, stroke volume, global average LV systolic wall stress, first derivative of LV pressure (LV dP/dt), and ejection fraction, whereas mean velocity of circumferential fiber shortening (V(cf)) and rate of change of VL short-axis diameter (LV dD/dt) rose but not significantly. At three levels of matched preload and afterload induced by the administration of graded doses of phenylephrine, V(cf), LV dD/dt, and LV dP/dt increased in hypertension compared with the same levels of preload and afterload before hypertension. When the loading conditions in the normotensive and hypertensive dogs were matched, either after ganglionic blockade or β-adrenergic blockade, both isovolumic and ejection-phase indexes of LV function remained similar before and after hypertension. Thus we conclude that 1) LV function in intact, conscious dogs with early hypertension is enhanced, and 2) the major mechanism for the increase in LV function involves the sympathetic nervous system.",
author = "Gelpi, {R. J.} and L. Hittinger and Fujii, {A. M.} and Crocker, {V. M.} and I. Mirsky and Stephen Vatner",
year = "1988",
month = "12",
day = "1",
language = "English (US)",
volume = "255",
journal = "American Journal of Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "6",

}

Sympathetic augmentation of cardiac function in developing hypertension in conscious dogs. / Gelpi, R. J.; Hittinger, L.; Fujii, A. M.; Crocker, V. M.; Mirsky, I.; Vatner, Stephen.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 255, No. 6, 01.12.1988.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Sympathetic augmentation of cardiac function in developing hypertension in conscious dogs

AU - Gelpi, R. J.

AU - Hittinger, L.

AU - Fujii, A. M.

AU - Crocker, V. M.

AU - Mirsky, I.

AU - Vatner, Stephen

PY - 1988/12/1

Y1 - 1988/12/1

N2 - To determine the alterations in left ventricular (LV) function and the mechanisms involved that occur during the development of perinephritic hypertension, dogs were instrumented with a miniature LV pressure transducer, aortic and left atrial catheters, and ultrasonic crystals to measure LV diameter in the short and long axes and wall thickness. At 2 wk after initiation of perinephritic hypertension, increases (P < 0.05) were observed in LV systolic pressure, LV end-diastolic pressure, both short- and long-axis end-diastolic diameters, calculated LV end-diastolic volume, stroke volume, global average LV systolic wall stress, first derivative of LV pressure (LV dP/dt), and ejection fraction, whereas mean velocity of circumferential fiber shortening (V(cf)) and rate of change of VL short-axis diameter (LV dD/dt) rose but not significantly. At three levels of matched preload and afterload induced by the administration of graded doses of phenylephrine, V(cf), LV dD/dt, and LV dP/dt increased in hypertension compared with the same levels of preload and afterload before hypertension. When the loading conditions in the normotensive and hypertensive dogs were matched, either after ganglionic blockade or β-adrenergic blockade, both isovolumic and ejection-phase indexes of LV function remained similar before and after hypertension. Thus we conclude that 1) LV function in intact, conscious dogs with early hypertension is enhanced, and 2) the major mechanism for the increase in LV function involves the sympathetic nervous system.

AB - To determine the alterations in left ventricular (LV) function and the mechanisms involved that occur during the development of perinephritic hypertension, dogs were instrumented with a miniature LV pressure transducer, aortic and left atrial catheters, and ultrasonic crystals to measure LV diameter in the short and long axes and wall thickness. At 2 wk after initiation of perinephritic hypertension, increases (P < 0.05) were observed in LV systolic pressure, LV end-diastolic pressure, both short- and long-axis end-diastolic diameters, calculated LV end-diastolic volume, stroke volume, global average LV systolic wall stress, first derivative of LV pressure (LV dP/dt), and ejection fraction, whereas mean velocity of circumferential fiber shortening (V(cf)) and rate of change of VL short-axis diameter (LV dD/dt) rose but not significantly. At three levels of matched preload and afterload induced by the administration of graded doses of phenylephrine, V(cf), LV dD/dt, and LV dP/dt increased in hypertension compared with the same levels of preload and afterload before hypertension. When the loading conditions in the normotensive and hypertensive dogs were matched, either after ganglionic blockade or β-adrenergic blockade, both isovolumic and ejection-phase indexes of LV function remained similar before and after hypertension. Thus we conclude that 1) LV function in intact, conscious dogs with early hypertension is enhanced, and 2) the major mechanism for the increase in LV function involves the sympathetic nervous system.

UR - http://www.scopus.com/inward/record.url?scp=0024238327&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024238327&partnerID=8YFLogxK

M3 - Article

VL - 255

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6135

IS - 6

ER -