Acidosis ; complications ; physiopathology ; Animals ; Aorta, Thoracic ; drug effects ; physiopathology ; Dopamine ; pharmacology ; In Vitro Techniques ; Male ; Rats ; Rats, Wistar ; Shock, Septic ; complications ; physiopathology ; Sympathomimetics ; pharmacology

BACKGROUND: Increased aortic stiffness is a independent risk factor of cardiovascular disease in patients with hypertension. Acute changes of the heart rate (HR) have been reported not to affect the aortic stiffness in pacing. However, it is unknown whether acute changes in HR caused by sympathomimetics can affect the aortic stiffness in patients with hypertension. We investigated the effect of acute changes in HR produced by isoproterenol on the aortic stiffness in 17 hypertensive patientss (mean age: 59 +/- 9 years). METHODS: All vasoactive drugs were discontinued at least 3 days before the study. The carotid-tofemoral pulse wave velocity (PWV) was measured by the foot-to-foot method. The pulse waves were recorded at the baseline and at every increase of HR by 5 to 10 bpm with a gradual increase of the dose of isoproterenol. The blood pressures and HR were measured simultaneously. For the analysis, HR, PWV, compliance (C), and compliance index (Ci) were converted as percent changes (delta) from the baseline values. Percent changes of the parameters of the aortic stiffness, i.e., delta PWV, delta C, and delta Ci, were grouped by every 10% increase in delta HR. RESULTS: There was no significant difference among groups in delta PWV, delta C and delta Ci (p> 0.05 for each of the group). The regression analysis showed no significant correlation of delta HR with delta PWV and delta C (r=0.18, 0.13 respectively, p> 0.05 for each). delta Ci had a poor correlation with delta HR (r=0.22, p< 0.05). However, only 4.6% of delta Ci could be referred to delta HR (r2=0.046). CONCLUSION: Aortic stiffness was not affected by acute changes in HR produced by isoproterenol which suggests that it is not necessary to consider acute changes in HR when measuring aortic PWV.
Aged ; Aorta/*drug effects ; Chest Pain/etiology ; Coronary Disease/complications ; Elasticity/drug effects ; Female ; Heart Rate/*drug effects ; Human ; Hypertension/complications/*physiopathology ; Isoproterenol/*pharmacology ; Linear Models ; Male ; Middle Aged ; Pulsatile Flow/physiology ; Sympathomimetics/*pharmacology

Whole gland perfusion technique was applied to rat parotid glands to assess whether amylase affects fluid secretion. Control perfusion without any secretagogue evoked no spontaneous secretion. Carbachol (CCh 1 microM) induced both amylase and fluid secretion with distinctive kinetics. Fluid secretion occurred constantly around 60 microL/g-min, whereas amylase secretion exhibited an initial peak, followed by a rapid decrease to reach a plateau. Isoproterenol (Isop 1 microM) alone did not induce fluid secretion although it evoked amylase secretion as measured in isolated perfused acini. Addition of Isop during CCh stimulation evoked a rapid and large rise in amylase secretion accompanied by small increase in oxygen consumption. Morphological observations carried out by HR SEM and TEM revealed exocytotic profiles following Isop stimulation. CCh stimulation alone seldom showed exocytotic profiles, suggesting a low incidence of amylase secretion during copious fluid secretion. Combined stimulation of CCh and Isop induced both vacuolation and exocytosis along intercellular canaliculi. These findings suggest that control of salivary fluid secretion is independent of the amylase secretion system induced by CCh and/or Isop.
Amylases/metabolism* ; Animal ; Carbachol/pharmacology ; Cholinergic Agonists/pharmacology ; In Vitro ; Isoproterenol/pharmacology ; Male ; Microscopy, Electron ; Microscopy, Electron, Scanning ; Oxygen Consumption/physiology ; Oxygen Consumption/drug effects ; Parotid Gland/ultrastructure ; Parotid Gland/secretion* ; Parotid Gland/enzymology* ; Perfusion ; Rats ; Rats, Wistar ; Saliva/metabolism* ; Sympathomimetics/pharmacology