摘要
In vitro,the effect of dailyzed plasma including parathyroid hypertensive factor (PHF) from SHR and parathyroid hormone (PTH) on 45Ca2+ uptake by vascular tissue was studied in the SD rats tail arteries incubated in the presence of Krebs-Heinsleit (K-H) buffer. The results showed that PHF significant increased 45Ca2+ uptake (3.90±0.56, n=12, P<0.001), but PTH significantly decreased 45Ca2+ uptake (1.08±0.51, n=16, P<0.001) as compared to control (2.20±0. 53, n=12). Increased doses of PTH resulted in decreasing of 45Ca2+uptake. The pressor mechanism of PHF may be due to stimulating calcium channel in smooth muscle cells,increasing 45Ca2+uptake and intracellular calcium in vascular tissues,whereas PTH acts as calcium antagonist,thereby reducing intracellular calcium level, expanding vascular vessels and decreasing blood pressure.
In vitro,the effect of dailyzed plasma including parathyroid hypertensive factor (PHF) from SHR and parathyroid hormone (PTH) on 45Ca2+ uptake by vascular tissue was studied in the SD rats tail arteries incubated in the presence of Krebs-Heinsleit (K-H) buffer. The results showed that PHF significant increased 45Ca2+ uptake (3.90±0.56, n=12, P<0.001), but PTH significantly decreased 45Ca2+ uptake (1.08±0.51, n=16, P<0.001) as compared to control (2.20±0. 53, n=12). Increased doses of PTH resulted in decreasing of 45Ca2+uptake. The pressor mechanism of PHF may be due to stimulating calcium channel in smooth muscle cells,increasing 45Ca2+uptake and intracellular calcium in vascular tissues,whereas PTH acts as calcium antagonist,thereby reducing intracellular calcium level, expanding vascular vessels and decreasing blood pressure.
基金
国家自然科学基金
