Angiotensin II-induced changes in cochlear blood flow and blood pressure in normotensive and spontaneously hypertensive rats

The present study assessed the short- and long-term effect of tempol, a membrane-permeable mimetic of superoxide dismutase, on renal medullary hemodynamics in spontaneously hypertensive rats (SHR). Tempol was given in the drinking water (1 mM) for 4 days or 7 wk (4–11 wk of age), and medullary blood flow (MBF) was measured over a wide range of renal arterial pressure by means of laser-Doppler flowmetry in anesthetized rats. In addition, the response of the medullary circulation to angiotensin II (5–50 ng · kg−1 · min−1 iv) was determined in SHR treated for 4 days with tempol. Compared with control SHR, short- and long-term treatment with tempol decreased arterial pressure by ∼20 mmHg and increased MBF by 35–50% without altering total renal blood flow (RBF) or autoregulation of RBF. Angiotensin II decreased RBF and MBF dose dependently (∼30% at the highest dose) in control SHR. In SHR treated with tempol, angiotensin II decreased RBF (∼30% at the highest dose) but did not alter MBF significantly. These data indicate that the antihypertensive effect of short- and long-term administration of tempol in SHR is associated with a selective increase in MBF. Tempol also reduced the sensitivity of MBF to angiotensin II. Taken together, these data support the idea that tempol enhances vasodilator mechanisms of the medullary circulation, possibly by interacting with the nitric oxide system. Increased MBF and reduced sensitivity of MBF to angiotensin II may contribute to the antihypertensive action of tempol in SHR.

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Different Effects on Inhibition of Cardiac Hypertrophy in Spontaneously Hypertensive Rats by Monotherapy and Combination Therapy of Adrenergic Receptor Antagonists and/or the Angiotensin II Type 1 Receptor Blocker under Comparable Blood Pressure Reduction

Hypertension Research ◽

10.1291/hypres.28.79 ◽

2005 ◽

Vol 28 (1) ◽

pp. 79-87 ◽

Cited By ~ 14

Author(s):

Takae ASAI ◽

Toshio KUSHIRO ◽

Hirotaka FUJITA ◽

Katsuo KANMATSUSE

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Combination Therapy ◽

Adrenergic Receptor ◽

Spontaneously Hypertensive Rats ◽

Blood Pressure Reduction ◽

Pressure Reduction ◽

Hypertensive Rats ◽

Spontaneously Hypertensive

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Arterial and arteriolar contributions to skeletal muscle functional hyperemia in spontaneously hypertensive rats

Journal of Applied Physiology ◽

10.1152/jappl.1995.78.1.93 ◽

1995 ◽

Vol 78 (1) ◽

pp. 93-100 ◽

Cited By ~ 6

Author(s):

J. M. Lash

Keyword(s):

Blood Flow ◽

Spontaneously Hypertensive Rats ◽

Muscle Blood Flow ◽

Muscle Contractions ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Wky Rats ◽

Tissue Po2 ◽

Wistar Kyoto ◽

Induced Changes

During contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR), arteriolar dilation is of normal magnitude but tissue PO2 is significantly depressed relative to normotensive [Wistar-Kyoto (WKY)] rats. This study examined the possibility that this low PO2 results from suppressed dilation of the upstream arterial feed vessels and a limitation of muscle blood flow. Contraction-induced changes in vascular resistances (R) and conductances (G) were calculated for upstream (Rup, Gup), microvascular (Rst, Gst), and downstream (Rdown, Gdown) vascular segments from measurements of pressure and flow in the rostral feed artery and vein. Feed arteries were smaller in SHR than in WKY rats at rest and after contractions (rest, 63.0 +/- 2.6 vs. 86.0 +/- 4.8 microns; 2 Hz 84.0 +/- 4.5 vs. 111.0 +/- 7.3 microns; 8 Hz, 130.0 +/- 5.9 vs. 144.0 +/- 7.1 microns). However, relative increases [times control (xCT)] in diameter and flow were greater in SHR (8 Hz diam, 2.080 +/- 0.072 vs. 1.690 +/- 0.042 xCT; 8 Hz flow, 15.700 +/- 2.057 vs. 8.170 +/- 0.752 xCT). In both groups, Rup and Rst decreased 60–70 and 85–90% after 2- and 8-Hz contractions, respectively. However, segmental vascular conductances increased more in SHR than in WKY rats (8 Hz: Gup, 18.50 +/- 3.76 vs. 8.00 +/- 1.26 xCT; Gst, 19.90 +/- 3.73 vs. 10.10 +/- 0.96 xCT; Gdown, 8.80 +/- 1.70 vs. 5.50 +/- 0.88 xCT). Therefore, upstream arterial dilation is not suppressed during muscle contractions in SHR, and deficits in muscle blood flow and oxygen delivery cannot account for the abnormally low tissue PO2 observed during muscle contractions in SHR.

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