scholarly journals The Changes of Renal Cortical Blood Flow in Spontaneously Hypertensive Rats

1983 ◽  
Vol 24 (5) ◽  
pp. 800-800
Author(s):  
Noboru Saito ◽  
Toshio Ozawa
Keyword(s):  
Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Cortical Blood Flow ◽  
Spontaneously Hypertensive ◽  
Renal Cortical Blood Flow

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

Cochlear blood flow in relation to age in normotensive and spontaneously hypertensive rats

1987 ◽  
Vol 104 (3-4) ◽  
pp. 243-250 ◽  
Author(s):  
Maria Hillerdal ◽  
Erik Borg ◽  
Berit Engstrom ◽  
Elisabeth Hultcrantz
Keyword(s):  
Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Cochlear Blood Flow ◽  
Spontaneously Hypertensive

Implication of renal perfusion pressure in stroke of spontaneously hypertensive rats

1980 ◽  
Vol 238 (3) ◽  
pp. H317-H324 ◽  
Author(s):  
A. Nagaoka ◽  
A. Shino ◽  
M. Shibota
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Cortex ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Hypertensive Rats ◽  
Cerebrovascular Lesions ◽  
Spontaneously Hypertensive ◽  
Renal Perfusion Pressure ◽  
Renal Changes ◽  
Renal Cortical Blood Flow

To elucidate the significance of hypertension associated with cerebrovascular lesions (CVL), renal perfusion pressure (RPP) was controlled by aortic clips of two different sizes in stroke-prone spontaneously hypertensive rats kept under normal or salt-loaded conditions. Tail and femoral arterial pressures (RPPs) in the mildly and severely clamped animals were reduced in proportion to the severity of the clamping. In contrast, carotid pressures in both clamped groups were significantly higher than that in the controls. Proteinuria and hyperreninemia accompanied by arteriolar changes in the renal cortex were observed in the controls prior to the onset of CVL. The renal changes were inhibited by both types of clamping. The onset of CVL was delayed by the mild clamping in salt-loaded animals, but accelerated by the severe clamping in both the normal and salt-loaded animals. Renal cortical blood flow was decreased only by the severe clamping. The results suggest that reduction in RPP and/or renal ischemia, which seems to be due to the hypertensive arteriolar changes in the renal cortex, may be related to the pathogenesis of CVL in the stroke-prone rats with or without hyperreninemia.

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