Main Article Content
Chronic exposure to high environmental temperature exacerbates sodium retention and worsens the severity of salt-induced hypertension in experimental rats via angiotensin receptor activation
Abstract
Background: There is paucity of information on how exposure to high environmental temperature interacts with high dietary salt to influence cardiovascular outcome in the face of global warming.
Method: This study investigated the impact of high environmental temperature (HET) on the cardio- renal indices of an animal model of hypertension (fed on high salt diet, HSD), and evaluated the effectiveness of angiotensin II receptor blocker (ARB), telmisartan, in modulating these indices. Fifty-six male Sprague Dawley rats (70-90g , 7 week old) were randomly assigned into seven groups of 8 rats, which include control rats (I), fed 0.3% NaCl diet; salt loaded rats (II), fed with 8% NaCl (high salt) diet; Heat rats (III), exposed to HET (37.5-38.5oC) 4 hours daily per week; salt loaded + Heat rats (IV), fed with 8% NaCl diet and exposed to HET daily. Next, salt loaded + ARB rats (V) , fed 8% NaCl diet and treated with telmisartan (30mg/kg); Heat +ARB rats, exposed to HET and treated with telmisartan (30mg/kg); salt loaded +HET+ARB rats (VI), fed with 8% NaCl diet, exposed to HET and treated with telmisartan (30mg/kg). Experiment lasted 8 weeks. Blood Pressure and heart rate were determined invasively and electrolytes by selective ion electrode method. Data analyzed using ANOVA, with P<0.05 significant.
Results: Systolic and Diastolic BP, Mean Arterial Pressure, Rate Pressures Product (RPP) (P<0.05), and plasma Na+ (P<0.05) were significantly higher with associated suppressed Na+ excretion (P<0.05) in salt loaded rats exposed to HET compared to rats fed a high salt diet alone. Telmisartan significantly attenuated the elevated blood (P<0.05) and RPP (P<0.05), in the HSD rats exposed to HET, with no corresponding reduction in the rats fed a HSD alone.
Conclusion: This indicates that chronic exposure to hot environment exaggerated cardiovascular response to high salt diet possibly via angiotensin II pathway with consequent enhanced ARB action.
Keywords: Angiotensin II receptor; high salt diet; hot environment; environmental temperature; heat exposure; hypertension