Ontogeny of neural and non-neural contributions to arterial blood pressure in spontaneously hypertensive rats.


Journal Article

Arterial blood pressure was measured directly by cannulation in anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats on postnatal Days 1, 5, 9, 20, 42, and 82-86. The time course for development of the following variables was established: resting diastolic and basal (after ganglionic blockade) pressure, the neural contribution to resting pressure (resting minus basal pressure), vascular reactivity to a noradrenergic agonist, methoxamine, and to endogenous sympathetic nerve terminal norepinephrine released by tyramine (maximum pressor response and ED50) and resting and basal heart rate. Resting diastolic pressure was higher in SHR compared to WKY by 24 hours after birth. In both strains, the increase in resting diastolic pressure with age was interrupted by a plateau period (Days 5-9 in SHR; Days 9-20 in WKY). Juxtaposition of the development curves was such that the interstrain differences in pressure were statistically significant in all periods studied except Days 5 and 9. Both basal and neurally mediated components of resting diastolic blood pressure were elevated in SHR compared to WKY. The magnitude of the interstrain difference in basal pressure remained constant during development while the magnitude of the neurally mediated component showed accelerated development through 42 days of age. Reactivity to methoxamine and tyramine was higher in SHR, but the magnitude of the difference did not change with age. Cardiac sympathetic tone was higher in SHR than WKY, but did not account for the increased resting diastolic pressure in SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Full Text

Duke Authors

Cited Authors

  • Smith, PG; Poston, CW; Mills, E

Published Date

  • January 1, 1984

Published In

Volume / Issue

  • 6 / 1

Start / End Page

  • 54 - 60

PubMed ID

  • 6693148

Pubmed Central ID

  • 6693148

International Standard Serial Number (ISSN)

  • 0194-911X

Digital Object Identifier (DOI)

  • 10.1161/01.hyp.6.1.54


  • eng

Conference Location

  • United States