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Summary 1. Hyperglycaemia is believed to be a major cause of diabetic vascular complications such as accelerated atherosclerosis. In order to elucidate the effect of hyperglycaemia on vascular response in spontaneously hypertensive rats (SHR), the natriuretic peptides receptor responses to vascular smooth muscle cells (VSMC) which are thought to suppress atherosclerosis were studied under high glucose (HG:22.2 mmol/L) conditions. 2. The total number of cells in SHR is higher and natriuretic peptides receptor response is smaller than that of cells in the Wistar-Kyoto (WKY) rat. Membrane bound protein kinase C (PKC) activity in HG or SHR is higher compared to that of cells in normal glucose (NG:5.6 mmol/L) or WKY. Cells cultured in HG for at least 2 passages had higher total cell number and receptor mediated cGMP formation were suppressed compared to cells cultured in NG both in SHR and WKY. Specific PKC inhibitor PKC (19–36) 1 μmol/L prevented HG induced suppression of natriuretic peptides response. 3. These results show that hyperglycaemia may be linked to suppressed natriuretic peptides receptor response which is caused by increased PKC activity both in WKY and SHR. This suppressed response may cause the accelerated atherosclerosis by hyperglycaemia.

1. Basal endothelin-1 (ET-1) production in mesangial cells of spontaneously hypertensive rats (SHR) was not different from that of Wistar-Kyoto (WKY) rats, although a trend toward increased ET-1 production was observed in these cells of SHR. 2. Thrombin and platelet-derived growth factor (PDGF) stimulated ET-1 production in a concentration-dependent manner in these cells of both rat strains, but thrombin- and PDGF-induced stimulation of ET-1 production were clearly greater in cells of SHR than WKY rats. 3. The protein kinase C (PKC)-activating phorbol ester, phorbol myristate acetate, stimulated ET-1 production in cells of both rat strains, but this stimulation was significantly greater in cells of SHR than in cells of WKY rats. 4. An inactive enantiomer of phorbol ester, 4alpha-PDD, had no effect on the ET-1 production in these cells of both rat strains. 5. Neither thrombin nor PDGF stimulated ET-1 production in PKC-depleted cells of both rat strains.

SUMMARY The hypertensive effect of bromocriptine in young (6 week old) spontaneously hypertensive rats (SHR) was studied. Blood pressure and plasma norepinephrine level in bromocriptine-treated SHR were significantly lower than those in vehicle-treated SHR after 3 weeks of treatment (5 mg/kg per day, i.p.), while no significant decrease of blood pressure or plasma norepinephrine level was observed after 2 weeks of treatment. These results suggest the involvement of sympathetic nervous system inhibition in the hypotensive effect of bromocriptine in SHR.

Intra-erythrocyte water, sodium and potassium contents were measured in spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt rats. In 12 week old SHR, the intra-erythrocyte water content was slightly but significantly lower than that in age-matched Wistar-Kyoto (WKY) rats. SHR also exhibited a significantly lower intra-erythrocyte potassium content, but sodium content tended to be elevated. Although sodium content was not correlated with the water content, potassium content was. In DOCA-salt hypertensive rats, the intra-erythrocyte sodium content was higher than that in age-matched normotensive Sprague-Dawley rats by about 33%, but the water and potassium contents were similar. There were no significant correlations between these parameters. These findings provide no evidence of water retention in erythrocytes from DOCA-salt rat or SHR even though intra-erythrocyte sodium content was increased.