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Updated: May 12, 2026

Simultaneous Electrocardiography Recording and Invasive Blood Pressure Measurement in Rats
Published on: January 31, 2019
Resistance training controls arterial blood pressure in rats with L-NAME- induced hypertension
Ayslan Jorge Santos de Araujo1, Anne Carolline Veríssimo dos Santos, Karine dos Santos Souza
1Departamento de Fisiologia, Universidade Federal de Sergipe, São Cristovão, Sergipe, Brasil.
Background:
Arterial hypertension is a multifactorial chronic condition caused by either congenital or acquired factors.
Objective:
To evaluate the effects of Resistance Training (RT) on arterial pressure, and on vascular reactivity and morphology, of L-NAME-treated hypertensive rats.
Methods:
Male Wistar rats (200 - 250 g) were allocated into Sedentary Normotensive (SN), Sedentary Hypertensive (SH) and Trained Hypertensive (TH) groups. Hypertension was induced by adding L-NAME (40 mg/Kg) to the drinking water for four weeks. Arterial pressure was evaluated before and after RT. RT was performed using 50% of 1RM, 3 sets of 10 repetitions, 3 times per week for four weeks. Vascular reactivity was measured in rat mesenteric artery rings by concentration-response curves to sodium nitroprusside (SNP); phenylephrine (PHE) was also used for histological and stereological analysis.
Results:
Resistance training inhibited the increase in mean and diastolic arterial pressures. Significant reduction was observed in Rmax (maximal response) and pD2 (potency) of PHE between SH and TH groups. Arteries demonstrated normal intima, media and adventitia layers in all groups. Stereological analysis demonstrated no significant difference in luminal, tunica media, and total areas of arteries in the SH and TH groups when compared to the SN group. Wall-to-lumen ratio of SH arteries was significantly different compared to SN arteries (p<0.05) but there was no difference when compared to TH arteries.
Conclusions:
RT was able to prevent an increase in blood pressure under the conditions in this study. This appears to involve a vasoconstrictor regulation mechanism and maintenance of luminal diameter in L-NAME induced hypertensive rats.
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