TY - JOUR
T1 - Plasma renin activity after acute heat exposure in nonacclimatized and naturally acclimatized man
AU - Finberg, J. P.M.
AU - Katz, M.
AU - Gazit, H.
AU - Berlyne, G. M.
PY - 1974/1/1
Y1 - 1974/1/1
N2 - Plasma renin activity (PRA) in residents of a semidesert zone was determined before and after exposure to high ambient temperature (50°C dry bulb, relative humidity 30%) for 90 min, by walking on a level treadmill at 4.7 km/h. These conditions caused a pronounced elevation of PRA, which was greater in the winter months that at the end of summer. No change occurred in PRA following the same treadmill walk at 25°C. The increase in PRA on heat exposure was not related to the degree of sweat loss, but was linearly correlated with the final heart rate. The degree of physiological strain produced was greater in winter than in summer. The increase in PRA was partially, but not completely, suppressed by replacing water and sodium chloride in advance of loss. Increased PRA in heat is suggested to be a result of sweat sodium loss, and renal nerve stimulation, which reflects the general visceral vasoconstriction compensating for extensive peripheral vasodilatation. Additionally, a reduction in splanchnic blood flow could lead to a reduced hepatic clearance of renin, resulting in a passive elevation of PRA.
AB - Plasma renin activity (PRA) in residents of a semidesert zone was determined before and after exposure to high ambient temperature (50°C dry bulb, relative humidity 30%) for 90 min, by walking on a level treadmill at 4.7 km/h. These conditions caused a pronounced elevation of PRA, which was greater in the winter months that at the end of summer. No change occurred in PRA following the same treadmill walk at 25°C. The increase in PRA on heat exposure was not related to the degree of sweat loss, but was linearly correlated with the final heart rate. The degree of physiological strain produced was greater in winter than in summer. The increase in PRA was partially, but not completely, suppressed by replacing water and sodium chloride in advance of loss. Increased PRA in heat is suggested to be a result of sweat sodium loss, and renal nerve stimulation, which reflects the general visceral vasoconstriction compensating for extensive peripheral vasodilatation. Additionally, a reduction in splanchnic blood flow could lead to a reduced hepatic clearance of renin, resulting in a passive elevation of PRA.
UR - http://www.scopus.com/inward/record.url?scp=0016153713&partnerID=8YFLogxK
U2 - 10.1152/jappl.1974.36.5.519
DO - 10.1152/jappl.1974.36.5.519
M3 - Article
C2 - 4826312
AN - SCOPUS:0016153713
SN - 8750-7587
VL - 36
SP - 519
EP - 523
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 5
ER -