1. SHR demonstrated exaggerated natriuresis with acute saline expansion. 2. RSNA in SHR was more inhibited than in WKY after acute saline expansion. 3. Therefore, RSNA in SHR may also be involved in the expression of exaggerated natriuresis with acute saline expansion.

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Na⁺, K⁺-ATPase activity was measured in cultured smooth muscle cells from the aorta of male WKY, SHRSR and SHRSP at the age of 3-months. Na⁺, K⁺-ATPase activity in SHRSR showed significantly higher than that in SHRSP. WKY showed intermediate activity between SHRSR and SHRSP. Na⁺, K⁺-ATPase activities were dose-dependently inactivated by fatty acid-free bovine serum albumin in all strains, especially in SHRSP. However, Mg⁺⁺-ATPase activities were not affected by the same treatment.

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As reported previously, captopril has an antihypertensive effect and suppresses the appearance and progression of sclerotic changes in the retinal arteriolar wall. This effect of captopril are probably brought by decrease of peripheral vascular resistance (Acta Soc. Ophthalmol. Jpn. 86: 227-238, 1982). Vascular lesions caused by sustained hypertension have been also confirmed in the tributaries of long posterior ciliary artery in SHRSP rats (Folia ophthalmol. Jpn. 30: 1907-1918, 1979).
The present study revealed that degenerative lesions occurred in the epithelia and blood vessels of ciliary body which has been thought to be responsible for the production of aqueous humor and for the nutrition of the crystalline lens. The lesions were more severe in the animal of poor controlled high blood pressure, at least in SHRSP, in accordance with the severity of cataract.
The lesions found in the ciliary body of SHRSP were probably induced by a damage of aqueous barrier following tissue ischemia as the hypertensive complication in the tributaries of long posterior ciliary artery. These findings might be a clue for the resolution of pathogenesis of human senile cataract.

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Retinal arteriolar recanalization was studied by fluorescein angiographic and pathological studies in SHRSP. In SHRSP, severe hypertension seemed to aggravate hemorrhagic cerebral infarction. Pathologically retinal arteriolar recanalization of the obstructed vessels caused more severe damage to the peripheral vessels than obstruction of the retinal arterioles only.

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GT was examined in SHRSR at various ages. The GT was the lowest at the age of 2-3 months and improved at the age of 5-6 months. GT in SHRSR fed on a high fructose diet (HFD) or a high sucrose diet (HSD) was significantly lower as compared to that in SHRSR fed on a normal diet (ND).

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One month-old male stroke-prone SHR were given 1% potassium chloride in drinking water and fed an ordinary low sodium diet throughout the life. There was no difference in the development of hypertension and the incidence of stroke compared to the control group. It was therefore suggested that potassium itself had no direct effect on blood pressure and the incidence of stroke but might affect them indirectly by counteracting dietary excess salt intake.

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The administration of normal diet containing 13.5% urea (in place of protein in the high protein diet) attenuated the development of severe hypertension and decreased the incidence of stroke in stroke-resistant SHR (SHRSR), when 1% NaCl solution was given to them.

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(1) Blood pressures and plasma cholesterol levels of crossbred offspring of M-SHRSP and SHC intermediated to their parental strains and came close to those of M-SHRSP or SHC through continuous backcrossings. (2) The rats, obtained through continuous successive selective brother-sister breeding for 4 generations by selecting rats with hypertension and noticeable hypercholesterolemia among the crossbred offspring of M-SHRSP and SHC, increased the tendencies to have hypertension, hypercholesterolemia and enlargement of kidneys.

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A high protein diet attenuates the development of hypertension. SHRSP, WKY and W were fed diets containing 6% to 30% protein. In comparison with W, the protein efficiency ratios (PER) in SHRSP and WKY were lower. Measurement of the absorption rates of essential amino acids in situ showed that absorption rates were less in SHRSP and WKY, and that in SHRSP the absorption of sulfurcontaining amino acids such as Taurin and Met were less than in WKY. These results suggest that stroke incidence rates can be satisfactorily lessened by improving the quality of protein in the diet.

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In SHR, a Ca²⁺ antagonist, Diltiazem significantly reduced the incidence of stroke. Thymidine incorporation into cultured smooth muscle cells was suppressed by 10^-4 M Diltiazem, so that strain difference disappeared. By autoradiogram Diltiazem was observed in cardiomyocyte organella and tended to concentrate finally on mitochondria.

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T-cell with depression and NTA production in Conv-SHR were marked when they were compared with SPF-SHR. When SPF-SHR were kept in a conventional breeding situation for 4 weeks, immunodepression and production of NTA were accelerated. Natural infection with microorganisms such as mouse hepatitis virus, Sendai virus and mycoplasma pulmonis appeared to be the main causative factors for the acceleration of immunologic abnormalities in SHR.

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T-cell dependent and independent resistance to L. monocytogenes were studied in SHR with congenital T-cell depression. The results presented here indicate that SHR have a nonspecifically activated macrophage system able to resist primary infection with L. monocytogenes but are lacking the interaction between T-cells and macrophages which are required for the acquisition of anti-Listeria immunity.

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