Summary
Young male spontaneously hypertensive rats were placed on a low (0.5 mmol/100 g), normal (13 mmol/100 g) or high (120 mmol/100 g) sodium diet for 6 weeks. Subsequent to the assessment of the basal blood pressure and heart rate in freely moving animals, the rats were pithed. In some of the pithed rats dose-response curves were constructed to exogenously administered noradrenaline (NA) and sympathetic nerve stimulation (SNS) through the pithing rod before and after the administration of an inhibitor of the neuronal uptake mechanism (desipramine, DMI, 0.5 mg/kg). In other pithed rats the SNS-induced (2 Hz) increase in plasma NA levels was assessed before and after the administration of clonidine (30μg/kg), an agonist at the prejunctional α2-adrenoceptors. We found that following the dietary intervention period the basal blood pressure and heart rate were higher in the high sodium group and lower in the low sodium group compared to values obtained in the control group. The neurogenic pressor responses clearly differed between the various diet groups. These differences could not be explained by differences in postjunctional responsiveness to exogenous NA. Rather, they were probably due to differences in the amount of transmitter at the synapse since the low sodium group was associated with decreased levels of plasma NA during SNS. Pretreatment with DMI potentiated the pressor responses, but largely to the same degree in the various diet groups, suggesting that there were no major differences in the function of the neuronal uptake mechanism. Hence, it is concluded that a low sodium diet causes an attenuation of transmitter release/impulse from the sympathetic nerve terminal. This reduction of transmitter release was not due to a facilitated prejunctional α2-adrenoceptor mediated autoinhibition; in contrast the inhibitory influence of clonidine on SNS-induced plasma NA levels was significantly smaller in the low sodium group.
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References
Abboud FM (1984) The sympathetic nervous system in hypertension. Clin Exper Hyper A 6 (1 and 2):43–60
De Champlain J, Krakhoff L, Axelrod J (1969) Interrelationships of sodium intake, hypertension and norepinephrine storage in the rat. Circ Res 24 (Suppl I):75–92
De Champlain J, van Amerigen M-R (1980) Evidence for the participation of sodium-sensitive pontine catecholamines in the maintenance of DOCA-sodium hypertensive rats. Clin Sci 59:259–262
Dietz R, Schömig A, Rascher W, Strasser R, Kübler W (1980) Enhanced sympathetic activity caused by salt loading in spontaneously hypertensive rats. Clin Sci 59:171–173
Dietz R, Schömig A, Rascher W, Strasser R, Kübler W, Gross F (1981) Stimulated sympathetic activity and increased vascular reactivity after high sodium diet. Circulation 62 (suppl III): 111–120
Ely DL, Weigand J (1983) Stress and high sodium effects on blood pressure and brain catecholamines in spontaneously hypertensive rats. Clin Exper Hyper A 5:1559–1587
Folkow B, Hallbäck M, Lundgren Y, Sivertsson R, Weiss L (1972) Importance of adaptive changes in vascular design for the establishment and maintenance of primary hypertension, as studied in man and in spontaneously hypertensive rats. In: Okamoto K (ed) Spontaneous hypertension; its pathogenesis and complications. Igaku Shoin Ltd, Tokyo, pp 103–114
Freis ED (1976) Salt, volume and the prevention of hypertension. Circulation 53:589–595
Gillespie JS, Muir TC (1967) A method of stimulating the complete sympathetic outflow from the spinal cord to blood vessels in the pithed rat. Br J Pharmacol Chemother 30:78–87
Gradin K, Elam M, Persson B (1985) Chronic salt loading and central adrenergic mechanism in the spontaneously hypertensive rat. Acta Pharmacol Toxicol 56:204–213
Hallman H, Farnebo L-O, Hamberger B, Jonsson G (1978) A sensitive method for the determination of plasma catecholamines using liquid chromatography with electrical detection. Anal Lett B 11:901–912
Keller R, Oke A, Mefford J, Adams R (1976) Liquid chromatographic analysis of catecholamines. Life Sci 19:995–1004
Louis WJ, Tabei S, Spector S, Sjoerdsma A (1969) Studies on the spontaneously hypertensive rat; Geneology effects of varying salt intake and kinetics of catecholamine metabolism. Circ Res 24 and 25 (suppl I): 1—93—102
Luft FC, Rankin J, Henry DP, Bloch R, Grim CE, Weiman AE, Murray RH, Weinberger MH (1979) Plasma and urinary norepinephrine values at extremes of sodium intake in normal man. Hypertension 1:261–266
Meldrum MJ, Xue C-S, Badino L, Westfall T (1985) Effect of sodium depletion on the release of norepinephrine from central and peripheral tissue of Wistar-Kyoto and spontaneously hypertensive rats. J Cardiovasc Pharmacol 7:59–65
Morgan TO, Myers JB (1981) Hypertension treated by sodium restriction. Med J Austr 2:396–397
Nakamura R, Gerold M, Thoenen H (1971) Relationship between the development of hypertension and the changes in norepinephrine turnover of peripheral and central adrenergic neurons. Naunyn-Schmiedeberg's Arch Pharmacol 271:157–169
Nilsson H, Ely D, Friberg P, Folkow B (1984) Effects of low and high Na diets on cardiovascular dynamics in normotensive WKY and hypertensive (SHR) rats. Abstract 10th Scientific Meeting of International Society of Hypertension, Interlaken, Switzerland, June 17–21,p 93
Nilsson H, Sjöblom N (1984) Extent of α2-receptor-mediated autoinhibition of vasoconstrictor nerve responses in mesenteric resistance vessels from normotensive and spontaneously hypertensive rats. Ibid p 84
Preuss HG, Fournier RD (1982) Effects of sucrose ingestion on blood pressure. Life Sci 30:879–886
Reid JL, Zivin JA, Kopin IJ (1975) Central and peripheral adrenergic mechanisms in the development of deoxycorticosteronesaline hypertension in rats. Circ Res 37:569–579
Rocchini AP, Cant JR, Barger AC (1980) Carotid sinus reflex in dogs with a low to high sodium intake. Am J Physiol 223:H196–202
Sanchez A, Pettinger WA (1981) Dietary sodium regulation of blood pressure and renal α1- and α2-receptors in WKY and SH rats. Life Sci 29:2795–2802
Takeshita S, Ferrario CM (1980) Effects of chronic sodium depletion on renal sympathetic activity in the anaesthetized dog. Physiologist 23:65
Takeshita A, Mark AL (1978) Neurogenic contribution to hindquaters vascoconstriction during high sodium intake in Dahl strain of genetically hypertensive rat. Hypertension 43 (suppl I): 1—86—91
Trolin G (1975) Involvement of α-adrenergic receptors at different levels of the central nervous system in the regulation of blood pressure and heart rate. Acta Physiol Scand suppl 430
Webb RC, Vanhoutte PM, Bohr DF (1981) Adrenergic neurotransmission in vascular smooth muscle from spontaneously hypertensive rats. Hypertension 3:93–103
Yamagouchi J, Kopin IJ (1979) Plasma catecholamine and blood pressure responses to sympathetic stimulation in pithed rats. Am J Physiol 237:H303–310
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Gradin, K., Dahlöf, C. & Persson, B. A low dietary sodium intake reduces neuronal noradrenaline release and the blood pressure in spontaneously hypertensive rats. Naunyn-Schmiedeberg's Arch. Pharmacol. 332, 364–369 (1986). https://doi.org/10.1007/BF00500088
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DOI: https://doi.org/10.1007/BF00500088