Excess Catecholamine Syndrome: Pathophysiology and Therapy^a

Abstract

In addition to genetic factors, lifestyle has a predominant influence on primary hypertension and noninsulin-dependent diabetic mellitus (NIDDM). We initiated studies using radiotelemetry for characterizing molecular events linked with excess calorie intake and psychologic stress. An increased calorie intake was associated with raised (p < 0.05) systolic and diastolic blood pressure as well as heart rate independent of day-night cycle. Sympathetic activity was in excess when related to the unchanged motility. The hyperkinetic hypertension is expected to result in adverse remodeling of resistance vessels and to aggravate insulin resistance. To examine adverse effects of psychological stress, rats were subjected to intermittent food pellet feeding. Urinary catecholamines and cardiac norepinephrine stores were increased (p < 0.05). The depressed (p < 0.05) rate of Ca2+ uptake of sarcoplasmic reticulum is expected to contribute to cellular Ca2+ overload. These lifestyle influences strengthen the notion of an excess catecholamine syndrome which requires selective reduction of sympathetic outflow of the brain by I1-receptor agonists.

Heart Rate and Heart‐Rate Variability Responses to Acute and Chronic Stress in a Wild‐Caught Passerine Bird

“…Chronic stress has been shown to increase cardiac disease in humans and laboratory mammals (McEwen 1998;Rupp 1999). Understanding the changes in HR regulation during stress in wild animals will be important in interpreting the consequences of stress in many free-living species.…”

“…However, either long-term activation of the stress response or exposure to frequent Stressors (i.e., chronic stress) is thought to be maladaptive and can lead to various physiological consequences (McEwen 1998). For example, cardiovascular consequences of excess catecholamines include hypertension, myocardial infarction, increased cardiac output, and arrhythmias (Rupp 1999). Several techniques for inducing chronic stress have been developed for laboratory mammals, especially rats (e.g., Kvetñansky and Mikulaj 1970;Porsolt et al 1977;Kant et al 1983;Willner et al 1991), but basic regulatory mechanisms are left unresolved by these studies.…”

Immune Modulation by Catecholamines - a Potential Mechanism of Cytokine Release in Heart Failure?

“…One possible mechanism could involve an enhanced transcription of the IL-6 gene via a cAMP responsive element in the promotor region [11]. The link between IL-6 and catecholamines may be relevant beyond overt heart failure since an excess catecholamine syndrome [13] is associated with the metabolic syndrome characterized by excess calorie intake, hypertension and noninsulin-dependent diabetes mellitus.…”

Pharmacological and biochemical modulation of stress markers by L-NAME and L-Ascorbic acid in chronic restraint model in Wistar rats

“…For example, the fight-or-flight response system, when chronically stimulated, can have a negative impact on cardiovascular health through excess catecholamines exposure leading to hypertension, myocardial infarction, increased cardiac output and arrhythmias. 5 In addition, because the fight-or-flight response is the animal's first line of defense to an acute stressor, such as the approach of a predator, changes in cardiac function due to chronic stress 6 may alter the animal's ability to mount the appropriate response that is crucial to survival. The adaptive aspects of the GC response also can prone maladaptive under chronic stress.…”