Studies in the past grant period indicated that the cerebral vasculature of adult (18-21 week) spontaneously hypertensive rats adapts to hypertension by hepertrophy of the vessel wall, vasoconstriction and a shift in the systemic arterial pressure range for near perfect autoregulation of blood flow from a normal range of 60-150 mmHg to 100-200 mmHg. Microvascular pressures in the vicinity of capillaries and the smallest venules were normal in SHR and there was no evidence of permanent or temporary closure of arterioles. In the proposed study, the protocol outlined will determine if in the earliest stages of hypertension, the SHR has vascular characteristics suitable for hypertensive life or if the vasculature is essentially normal in early life but must progressively adapt as the systemic hypertension develops. Mammalian intestinal villi have three major shapes and vascular architecture patterns which are represented in rats, rabbits and cats. These anatomical characteristics in concert with the transport characteristics of the mucosal epithelia and possible differences in counter-current exchange and multiplication system efficiency could result in very different conditions in tissue PO2 and concentrations of absorbed materials along the villus shaft in various species. The purpose of outlined protocols is to determine if villus tissue conditions are dominated by the transport and oxygen consumption characteristics of the mucosal epithelia or if the counter-current system establishes villus apical to base PO2, concentration or osmotic gradients. In addition, pressures in villus capillaries of rats, rabbits and cats will be measured at rest and during maximum absorptive hyperemia to determine if the normally low villus capillary pressure, 12-16 mmHg, at rest is maintained during hyperemia and thereby assists fluid absorption. By comparing villus tissue chemical conditions and microvascular characteristics in three different species, it will be possible to determine if intestinal villus physiology during absorption is similar in mammalian species or dependent upon the unique anatomical and microvascular characteristics of each species.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL020605-11
Application #
3336183
Study Section
Cardiovascular and Pulmonary Research B Study Section (CVB)
Project Start
1977-04-01
Project End
1989-03-31
Budget Start
1987-04-01
Budget End
1989-03-31
Support Year
11
Fiscal Year
1987
Total Cost
Indirect Cost
Name
Indiana University-Purdue University at Indianapolis
Department
Type
Schools of Medicine
DUNS #
005436803
City
Indianapolis
State
IN
Country
United States
Zip Code
46202
Bohlen, Harold Glenn (2015) Nitric oxide and the cardiovascular system. Compr Physiol 5:808-23
Bohlen, H Glenn (2013) Is the real in vivo nitric oxide concentration pico or nano molar? Influence of electrode size on unstirred layers and NO consumption. Microcirculation 20:30-41
Bohlen, H Glenn (2011) Rapid and slow nitric oxide responses during conducted vasodilation in the in vivo intestine and brain cortex microvasculatures. Microcirculation 18:623-34
Zhou, Xiaosun; Bohlen, H Glenn; Unthank, Joseph L et al. (2009) Abnormal nitric oxide production in aged rat mesenteric arteries is mediated by NAD(P)H oxidase-derived peroxide. Am J Physiol Heart Circ Physiol 297:H2227-33
Bohlen, H G; Zhou, X; Unthank, J L et al. (2009) Transfer of nitric oxide by blood from upstream to downstream resistance vessels causes microvascular dilation. Am J Physiol Heart Circ Physiol 297:H1337-46
Payne, Gregory A; Bohlen, H Glenn; Dincer, U Deniz et al. (2009) Periadventitial adipose tissue impairs coronary endothelial function via PKC-beta-dependent phosphorylation of nitric oxide synthase. Am J Physiol Heart Circ Physiol 297:H460-5
Zhou, Xiaosun; Bohlen, H Glenn; Miller, Steven J et al. (2008) NAD(P)H oxidase-derived peroxide mediates elevated basal and impaired flow-induced NO production in SHR mesenteric arteries in vivo. Am J Physiol Heart Circ Physiol 295:H1008-H1016
Bauser-Heaton, Holly D; Song, Jin; Bohlen, H Glenn (2008) Cerebral microvascular nNOS responds to lowered oxygen tension through a bumetanide-sensitive cotransporter and sodium-calcium exchanger. Am J Physiol Heart Circ Physiol 294:H2166-73
Payne, Gregory A; Borbouse, Lena; Bratz, Ian N et al. (2008) Endogenous adipose-derived factors diminish coronary endothelial function via inhibition of nitric oxide synthase. Microcirculation 15:417-26
Pezzuto, Laura; Bohlen, H Glenn (2008) Extracellular arginine rapidly dilates in vivo intestinal arteries and arterioles through a nitric oxide mechanism. Microcirculation 15:123-35

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