title: Altered vascular resistance properties and acute pressure-natriuresis mechanism in neonatal and weaning spontaneously hypertensive rats.
abstract: Although it has been extensively scrutinized, the factor(s) involved in the initiation and development of hypertension in spontaneously hypertensive rats (SHRs) remains unresolved. The objective of the present study was to determine whether, early in development, the causal mechanism(s) for the development of hypertension in young SHRs involves an integration of 2 processes, specifically an upregulation of structurally based vascular resistance properties and a rightward shift in the hemodynamic component of pressure-natriuresis. Mean arterial pressure was determined in conscious 4-week-old SHRs and Wistar-Kyoto rats via previously implanted aortic catheters. Structurally based hindlimb vascular resistance properties were assessed in 2- and 4-week-old SHRs and Wistar-Kyoto rats. Renal interstitial hydrostatic pressure was measured after short-term manipulations of renal arterial pressure (RAP) in 4-week-old, anesthetized rats. Although mean arterial pressure in conscious SHRs (113±5 mm Hg) and Wistar-Kyoto rats (110±6 mm Hg) was not significantly different at 4 weeks of age, SHRs at 2 and 4 weeks of age already had increases in structurally based vascular resistance properties of ≈30% above age- and weight-matched Wistar-Kyoto rats. Furthermore, the acute RAP-renal interstitial hydrostatic pressure relationship was found to be linear in both strains, and the temporal coupling of the stimulus to response was rapid; that is, renal interstitial hydrostatic pressure responses to changes in RAP were <2 s. Although the slope of the RAP-renal interstitial hydrostatic pressure relationship was not significantly different between strains, the relationship was significantly shifted (18%) to higher RAPs in SHRs. These results suggest that alterations in both vascular structure and renal function in young SHRs occur before elevations in mean arterial pressure.
authors.affiliation: Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
authors.forename: Marina
authors.initials: M
authors.lastname: Komolova
authors.forename: Peter
authors.initials: P
authors.lastname: Friberg
authors.forename: Michael A
authors.initials: MA
authors.lastname: Adams
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001794:Blood Pressure / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D006614:Hindlimb / Q000098:blood supply*; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D023421:Models, Animal; D009318:Natriuresis / Q000502:physiology*; D011311:Pressoreceptors; D011312:Pressure; D011897:Random Allocation; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012680:Sensitivity and Specificity; D014655:Vascular Resistance / Q000502:physiology*; D014886:Weaning