Sympathectomy and cardiovascular spectral components in conscious normotensive rats.
We examined the extent to which sympathetic influences are reflected by spectral powers of blood pressure and pulse interval in specific frequency bands in spontaneously behaving Wistar-Kyoto rats subjected to continuous intraarterial blood pressure recording. The rats were pretreated with 6-hydroxydopamine (150 mg/kg twice in 1 week, n = 19) to produce chemical sympathectomy or received vehicle (n = 15). In the sympathectomized group, additional monitoring sessions were performed with rats under alpha-adrenergic receptor blockade with phenoxybenzamine (n = 8), beta-receptor blockade with propranolol (n = 7), or cholinergic receptor blockade with atropine (n = 8). Blood pressure signals were analyzed by a computer to calculate spectral powers (fast Fourier transform) in the low-frequency (0.025 to 0.1 Hz), mid-frequency (0.1 to 0.6 Hz), and high-frequency (0.8 to 3.0 Hz) bands. In sympathectomized rats, low-frequency power of blood pressure was 70% greater than in intact rats, whereas mid-frequency power was 60% smaller (P < .05 for both) and high-frequency power was unchanged. High-frequency power of pulse interval was also unchanged in sympathectomized rats, whereas low- and mid-frequency powers were reduced by approximately 50% (P < .05). No further alterations in spectral powers were observed by adding alpha- or beta-adrenergic blockade to sympathectomy, whereas adding cholinergic blockade caused a striking reduction in all pulse interval powers. Thus, mid-frequency blood pressure power depends on sympathetic but also to a substantial extent on nonsympathetic influences. Sympathetic influences do not contribute to low-frequency blood pressure power, having instead a restraining effect. The low- and mid-frequency pulse interval powers depend on both sympathetic and vagal influences. Thus, no blood pressure or pulse interval power in the mid- and low-frequency ranges can be regarded as a specific marker of sympathetic activity.
Daffonchio
A
A
Centro Fisiologia Clinica e Ipertensione, Ospedale Maggiore, Milano, Italy.
Franzelli
C
C
Radaelli
A
A
Castiglioni
P
P
Di Rienzo
M
M
Mancia
G
G
Ferrari
A U
AU
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D008297:Male; D010276:Parasympatholytics / Q000494:pharmacology; D011674:Pulse; D051381:Rats; D011921:Rats, Inbred WKY; D012815:Signal Processing, Computer-Assisted; D013563:Sympathectomy, Chemical; D013564:Sympathetic Nervous System / Q000502:physiology*
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D010276:Parasympatholytics