Psychophysiology of arterial baroreceptors and the etiology of hypertension
Introduction
The central nervous system receives continuous information about changes in blood pressure through the pressure or baroreceptors. They play an essential role in blood pressure regulation. Investigating the physiological characteristics of the arterial baroreceptors in dogs, the physiologist Koch (1932) made unexpected observations; baroreceptor stimulation not only led to cardiovascular regulatory responses, but when prolonged, put the animal to sleep. The ancient Greek scholars must have been aware of this effect of baroreceptors in the carotid artery, as ‘carotis’ means ‘deep sleep’. The other name of this artery, ‘arteria lethargica’ points to the calming effect, a massaging or rubbing in the region of the carotid sinus (which stimulates the baroreceptors) may have.
Here, we review the extrahomeostatic effects of baroreceptor firing, i.e., effects that go beyond immediate regulation of blood pressure. In particular, different methods of experimental baroreceptor stimulation and the link to hypertension are discussed in a model describing how learning mechanisms can contribute to hypertension.
Section snippets
The arterial baroreceptors
A variety of receptors transmits information about cardiovascular status to the brain. The pressure receptors that respond to the tension of the arterial walls, the arterial baroreceptors, are located near the output of the heart (in the aortic branch) and in the carotid arteries where they monitor the pressure in the vessels that are essential for the brain's blood supply (Fig. 1).
There exist a number of histologically discriminable baroreceptors in the wall of the arteria carotis communis (
Techniques to alter baroreceptor activity in humans
In order to portray the direct consequences of baroreceptor firing on central nervous processes and behavior, experimental approaches are needed that vary baroreceptor activity as the independent variable and provide monitoring of neurophysiological and behavioral dependent measures. Techniques, which allow the manipulation of baroreceptor activity, vary with respect to their specificity. A specific manipulation technique handles the independent variable (here the baroreceptor activity) but has
Extrahomeostatic baroreceptor effects in humans
An increase in arterial blood pressure stimulates the arterial baroreceptors which in turn elicit the baroreceptor reflex via the neurons in the solitary tract: a reduction in cardiac output and in peripheral resistance reduces blood pressure towards its original level. This reflex may be inhibited through peripheral processes, for example, under conditions of high metabolic demand. In addition, higher brain structures modulate this reflex arc, for instance when threat is detected and fight or
Pain and the cardiovascular system
Considerable evidence suggests a link between hypertension and hypoalgesia. A weak but consistent correlation indicates that hypertensive humans as well as hypertensive animals are less likely to perceive pain than are normotensive subjects. Such correlational observations do not allow a determination of whether hypoalgesia is a consequence or a cause of hypertension or whether both hypertension and hypoalgesia result from a third process (e.g., an alteration in endogenous opioid system;
Experimentally induced hypertension and pain (animal studies)
In contrast to human correlational studies, Zamir and Segal (1979) performed animal studies, which allowed for stringent experimental control of blood pressure. They produced renal hypertension in male rats by occluding the left renal artery and leaving the right kidney intact. They also included a group of sham operated rats and a third group of rats in which the left renal artery was totally constricted so that the kidney became atrophied and could no longer produce renin. After these
Significance of the baroreceptor–brain circuitry for a model of learned hypertension
Based on the observation of arousal and pain dampening exerted through baroreceptor activation, Dworkin, Rau, Elbert and colleagues (Dworkin, 1988, Rau and Elbert, 1993, Elbert et al., 1994, Dworkin et al., 1994, Dworkin et al., 2000) advanced the model of ‘learned hypertension’. This theory predicts that learning mechanisms, and operant conditioning in particular, contribute to blood pressure elevations with a possibly catastrophic outcome. The reduction in pain and stress constitutes a
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2022, International Journal of PsychophysiologyCitation Excerpt :Blunted cardiovascular reactivity may also promote pain, as phasic cardiovascular increases, especially in BP, produce antinociceptive effects (Bruehl and Chung, 2004) through the central nervous inhibition mediated by baroreceptors afferents (Davydov, 2021; Rau and Elbert, 2001; Reyes del Paso et al., 2014). This generalized central inhibitory effect mediated by baroreceptor stimulation is manifested in well-known phenomena, i.e., stress-related analgesia or hypertension-induced hypoalgesia (Bruehl and Chung, 2004; Davydov, 2021; Rau and Elbert, 2001; Reyes del Paso et al., 2014), and is relevant to the BP-emotional dampening hypothesis (Davydov et al., 2012; Delgado et al., 2014; McCubbin et al., 2011) by which increases in cardiovascular activity inhibit negative stimuli processing and emotional expression. Furthermore, deficient autonomic responses have found to be linked to decreased immune functioning (Benarroch, 2009; Ottaviani et al., 2009) as well as to orthostatic intolerance, frequently observed in FM (El-Sawy et al., 2012; Furlan et al., 2005; Raj et al., 2000; Staud, 2008).
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