Waiting a few extra minutes before measuring blood pressure has potentially important clinical and research ramifications.

Office blood pressure (BP) is recommended to be measured after 5 min of seated rest, but it may decrease for 10 min of seated rest. This study aimed to determine the change (and its clinical relevance) in brachial and central BP from 5 to 10 min of seated rest. Office brachial and central BP (measured after 5 and 10 min), left ventricular (LV) mass index, 7-day home and ambulatory BP were measured in 250 participants with treated hypertension. Office brachial and central BP were significantly lower at 10-min compared with 5-min BP (P<0.001). Seven-day home systolic BP (SBP) was significantly lower than office SBP measured at 5 min (P<0.001), but was similar to office SBP at 10 min (P=0.511). From 5 to 10 min, the percentage of participants with controlled BP increased and the percentage of participants with high central pulse pressure (PP) decreased (P<0.001). Moreover, brachial and central PP were significantly correlated with LV mass index measured at 10 min (r=0.171, P=0.006 and r=0.139, P=0.027, respectively), but not at 5 min (r=0.115, P=0.068 and r=0.084, P=0.185, respectively). BP recorded after 10 min is more representative of true BP control. These findings have relevance to appropriate diagnosis of hypertension and design of clinical trials.

Persistent elevation of central pulse pressure during postural stress in patients with type 2 diabetes mellitus.

An abnormal increase or decrease in blood pressure (BP) in response to postural stress is associated with increased risk of developing hypertension and stroke. However, the haemodynamic responses contributing to changes in central BP with postural stress are not well characterised. We aimed to determine this in controls compared to patients with type 2 diabetes mellitus (T2DM), whom we hypothesised would have an abnormal postural response. 41 participants (20 control, 21 T2DM) underwent measurement of brachial and central BP (by radial tonometry), with simultaneous bioimpedance cardiography (to determine stroke volume (SV) and cardiac output (CO)) and heart rate variability in seated and standing postures. Systemic vascular resistance (SVR; mean arterial pressure/CO), and arterial elastance (EA; end systolic pressure/SV) were calculated. Postural changes were defined as seated minus standing values. Central pulse pressure (PP) was higher in patients with T2DM and did not change from seated-to-standing positions, whereas there was a significant decrease upon standing in controls (P<0.05). The change in central systolic BP (SBP) correlated with change in SVR and EA in controls (r=0.67 and 0.68, P<0.05, respectively), but not in patients with T2DM (r=-0.05 and r=0.03, P>0.05, respectively). SV was the only significant correlate of change in central SBP in T2DM patients (r=0.62, P<0.05) and this was not observed in controls (r=-0.08 P>0.05). We conclude that central haemodynamic responses to postural stress are altered in patients with T2DM and result in persistent elevation of central PP while standing. This may contribute to increased cardiovascular risk associated with T2DM.

Differential inhibition by ethanol of norepinephrine- and clonidine-induced emesis in cats.

The effect of acute ethanol administration into the cerebral ventricles on the unanesthetized cat upon emesis produced by norepinephrine and clonidine injected similarly as well as upon emesis evoked by copper sulfate given orally was compared and investigated. Ethanol inhibited the norepinephrine- and clonidine-induced emesis. The inhibitory effect of ethanol occurred after a transient and inconsistent emetic action of the drug. Norepinephrine-induced emesis was about 12 times more sensitive than clonidine-induced emesis to the inhibitory effect of ethanol. In addition, norepinephrine-, but not clonidine-induced emesis was abolished after ablation of the area postrema. On the contrary, intracerebroventricular ethanol had virtually no effect on emesis caused by intragastric copper sulfate. The inhibitory effect of ethanol is ascribed to an action on alpha-2 adrenoceptors within the area postrema and on imidazoline-preferring sites and/or muscarinic cholinoceptors outside the area postrema, but not on the emetic region of the brainstem reticular formation. It follows then that ethanol can differentiate alpha-2 adrenoceptors from imidazoline-preferring sites and/or muscarinic cholinoceptors in the brain of the cat.

Selective effect of ethanol on norepinephrine- and nicotine-induced emesis in cats.

The effect of acute ethanol administration into the cerebral ventricles of the unanesthetized cat upon emesis produced by norepinephrine and nicotine injected similarly was investigated. Ethanol inhibited the norepinephrine- and nicotine-induced emesis. The inhibitory effect of ethanol occurred after a transient and inconsistent emetic action of the drug. Ethanol was about 10 times more potent inhibiting the emesis caused by nicotine. On the other hand, intracerebroventricular ethanol had virtually no effect on emesis produced by intragastric copper sulfate. The inhibitory effect of ethanol is ascribed to an action on alpha-noradrenergic and nicotinic receptors in the area postrema. Differential responses to ethanol most probably reflect the microenvironment of alpha-noradrenergic and nicotinic synapses in the area postrema of the cat.