title: Arterial spontaneous rhythmic contractile activity in humans and rats: spectral analysis and regulatory mechanisms.
abstract: OBJECTIVE
  Many experimental observations have demonstrated the presence of spontaneous cyclic vasomotor activity (CVA) in large and small arteries. This study aimed to evaluate the characteristics of spontaneous CVA in rat and human resistance arteries, and to investigate its possible interference with the evaluation of sympathetic activity by means of spectral analysis of blood pressure in vivo.
  
  
  RESULTS
  In study 1 we examined small mesenteric arteries of spontaneously hypertensive rats and Wistar-Kyoto rats, as well as small omental arteries of normotensive subjects and hypertensive patients (Mulvany and Halpern technique). CVA was enhanced by the agonists of nitric oxide release, and was abolished by the inhibitors of nitric oxide or cyclic GMP synthesis. A potassium channel, which is barium- and zinc-sensitive and tetraethylammonium-insensitive, seems to play a crucial role in the genesis of CVA. In rats and in humans the frequency of CVA fell exactly in the frequency band ('low frequencies') of power spectral analysis of blood pressure usually considered to be an 'index of sympathetic activity'. In study 2, a power spectral analysis of blood pressure variability before and after intra-arterial infusion of noradrenaline or acetylcholine was performed in 18 patients with mild-to-moderate hypertension. The absolute and normalized spectral power of the low-frequency systolic blood pressure peak increased remarkably after noradrenaline and acetylcholine infusion, while its central frequency shifted from 0.10 Hz to approximately 0.06 Hz, exactly the frequency of CVA observed in vitro.
  
  
  CONCLUSIONS
  A potassium channel appears to be involved in the genesis of CVA. Also, CVA might contribute to the blood pressure variability independently of the autonomic nervous system activity, and thus probably plays a role in the genesis of the low-frequency peak in the rat and in humans.
authors.affiliation: Chair of Semeiotica e Metodologia Medica, University of Brescia, Italy.
authors.forename: D
authors.initials: D
authors.lastname: Rizzoni
authors.forename: M
authors.initials: M
authors.lastname: Castellano
authors.forename: E
authors.initials: E
authors.lastname: Porteri
authors.forename: G
authors.initials: G
authors.lastname: Bettoni
authors.forename: P
authors.initials: P
authors.lastname: Muiesan
authors.forename: M L
authors.initials: ML
authors.lastname: Muiesan
authors.forename: S M
authors.initials: SM
authors.lastname: Giulini
authors.forename: A
authors.initials: A
authors.lastname: Cinelli
authors.forename: M
authors.initials: M
authors.lastname: Salvetti
authors.forename: E
authors.initials: E
authors.lastname: Agabiti Rosei
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000328:Adult; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D001341:Autonomic Nervous System / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013057:Spectrum Analysis; D013566:Sympathomimetics / Q000494:pharmacology; D014666:Vasomotor System / Q000187:drug effects / Q000502:physiology*
chemical_list: D013566:Sympathomimetics; D000109:Acetylcholine; D009638:Norepinephrine