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This study addresses the hypothesis that atrial natriuretic factor (ANF) is a primary vasodilator, which reduces arterial pressure directly and increases total peripheral resistance secondarily by reflex mechanisms. The effects of 30-minute infusions of ANF (0.3 micrograms/kg/min i.v.) were examined in conscious dogs, rats, and monkeys before and after ganglionic blockade with hexamethonium. In seven intact, conscious dogs, ANF reduced mean arterial pressure by 7 +/- 1% and cardiac output by 19 +/- 3% and increased total peripheral resistance by 15 +/- 3%. After ganglionic blockade, ANF reduced mean arterial pressure by 7 +/- 2% but still increased total peripheral resistance by 15 +/- 3%. Similar results were observed in four dogs with total cardiac denervation and in six dogs with arterial baroreceptor denervation. Furthermore, in two dogs, combined ganglionic and alpha 1-adrenoceptor blockades failed to alter the rise in total peripheral resistance observed with ANF. In six intact, conscious rats, ANF reduced mean arterial pressure by 8 +/- 2% and cardiac output by 27 +/- 2% and increased total peripheral resistance by 27 +/- 5%. After ganglionic blockade, ANF still increased total peripheral resistance by 13 +/- 3%. In six intact, conscious monkeys, ANF reduced mean arterial pressure by 14 +/- 2% and cardiac output by 26 +/- 3% and increased total peripheral resistance by 17 +/- 3%. However, after ganglionic blockade. ANF decreased total peripheral resistance by 11 +/- 2%. These data provide evidence for a fundamental species difference in the vascular actions of ANF. In conscious dogs, ANF elicits "direct" vasoconstriction, which increases total peripheral resistance, even in the presence of denervation of reflexes or autonomic blockade. In conscious rats, ANF elicits both direct and reflexly mediated vasoconstriction. In conscious monkeys, although a component of direct vasoconstriction may also be present, the most prominent component appears to be reflexly mediated, since it was abolished by ganglionic blockade.
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
October 1990,
The American journal of physiology,
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
November 1986,
The American journal of physiology,
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
May 1999,
The American journal of physiology,
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
April 1986,
Hypertension (Dallas, Tex. : 1979),
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
January 1990,
Pflugers Archiv : European journal of physiology,
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
January 1985,
Hypertension (Dallas, Tex. : 1979),
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
December 1988,
Clinical and investigative medicine. Medecine clinique et experimentale,
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
April 1990,
American journal of hypertension,
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
April 1985,
Life sciences,
Y T Shen, and
M A Young, and
J Ohanian, and
R M Graham, and
S F Vatner
April 1985,
The American journal of physiology,
