Effects of high and low sodium diets on the resistance vessels and their adrenergic vasoconstrictor fibre control in normotensive (WKY) and hypertensive (SHR) rats

• Published in: Acta physiologica Scandinavica 1985-10, Vol.125 (2), p.323-334
• Main Authors: NILSSON, HOLGER, ELY, DANIEL, FRIBERG, PETER, KARLSTRÖM, GÖRAN, FOLKOW, BJÖRN
• Format: Article
• Language: English
• Subjects: Adrenergic beta-Antagonists - pharmacology; Adrenergic Fibers - physiology; Adrenergic transmitter release; Animals; Applied sciences; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Diet, Sodium-Restricted; Electric Stimulation; Exact sciences and technology; Experimental diseases; Female; Hindlimb - blood supply; hypertension; Male; Medical sciences; Muscle Contraction - drug effects; Muscle, Smooth, Vascular - physiology; Norepinephrine - pharmacology; Other techniques and industries; Perfusion; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Sodium - pharmacology; sodium and adrenergic nerve function; sodium intake; sympathetic nervous system; sympathetic neuro-effector function; Vascular Resistance - drug effects; Vasoconstriction - drug effects
• ISSN: 0001-6772; 1365-201X
• DOI: 10.1111/j.1748-1716.1985.tb07722.x

As part of our studies in normotensive (WKY) and hypertensive (SHR) rats concerning the cardiovascular effects of 240‐fold variations in sodium (Na) intake, the present experiments explore how vascular design, smooth‐muscle sensitivity to noradrenaline and adrenergic vasoconstrictor fibre function are affected. In vitro comparisons were performed on pair‐perfused hindquarter vascular beds and on paired small mesenteric arteries (diameter 150–200 μM), using a two‐vessel Mulvany‐Halpern myograph. Preparations were taken from WKY and SHR which between 5 and 12–13 weeks of age were on ‘low’ (LNa, 0.5), ‘control’ (CNa, 5), ‘high’ (HNa, 50) or ‘very high’ (vHNa, 120 mmol Na 100 g‐1 food) sodium diets. Structural vascular adaptation occurred only when arterial pressure was altered (only in LNa SHR). In both preparations smooth‐muscle sensitivity and dose‐response curves to noradrenaline remained unaffected by the Na diets. However, in both LNa groups the frequency‐response curves to vasoconstrictor fibre stimulation in the small arteries were displaced to the right of the CNa one, with generally attenuated responses, while the curves of particularly the vHNa arteries were displaced to the left, with enhanced responses. Inhibition of NaKATPase by ouabain particularly enhanced the neurogenic responses, but to similar extents in all Na groups. Thus, low sodium intake apparently reduces the transmitter release/impulse in adrenergic neurons, while it increases the transmitter stores. High sodium intake has the opposite effects. These adaptations of adrenergic neuronal function may be one of the most important long‐term consequences of altered sodium intake.