Centrally Acting Antihypertensive Agents: An Update

Sica, Domenic A.

doi:10.1111/j.1524-6175.2007.07161.x

Cited by 93 publications

(80 citation statements)

References 42 publications

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“…In some countries, β-adrenoceptor blockers are prescribed to block 26 sympathetically mediated release of renin from the kidney (Wong et al, 2016). Calcium channel 27 blockers and α1-adrenoceptor antagonists reduce vascular resistance (Cubeddu, 1988;Tocci et al, 28 2015), while centrally-acting sympatholytic drugs such as the α2-adrenoceptor agonist clonidine and 29 the imidazoline receptor agonist moxondine, lower sympathetic activity (Sica, 2007). The clinician 30 will typically follow a nationally-agreed protocol for drug type, dose and sequence/combinations 31 …”

Section: Do We Need New Treatments For Hypertension?mentioning

confidence: 99%

Evaluating the carotid bodies and renal nerves as therapeutic targets for hypertension

McBryde

Hart

Ramchandra

et al. 2017

Autonomic Neuroscience

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University of Bristol -Explore Bristol Research General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms Despite the plethora of current treatment options, hypertension remains a difficult condition to 12 adequately control, and there is a pressing need for novel therapeutic strategies. The carotid body 13 has recently become the focus of considerable interest as a potential novel treatment target in 14 essential hypertension. Herein, we appraise the current literature suggesting that the carotid body 15 plays an important causative role to generate sympathetic overactivity and drive increases in arterial 16 pressure, in animal models of hypertension. We also review evidence from human studies showing 17 cardiovascular benefits to the transient inactivation, or surgical removal of carotid bodies, and 18 evaluate the potential benefits of pre-screening to identify patients likely to respond to carotid 19 body-targeted therapy. Finally, given that a high proportion of patients who have undergone renal 20 nerve ablation procedures remain hypertensive, we examine whether the renal nerves are necessary 21 for the drop in blood pressure seen with carotid body removal. 22 23

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Section: Do We Need New Treatments For Hypertension?mentioning

confidence: 99%

Evaluating the carotid bodies and renal nerves as therapeutic targets for hypertension

McBryde

Hart

Ramchandra

et al. 2017

Autonomic Neuroscience

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“…This induces central inhibition of norepinephrine (NE) via the attenuation of NE release from terminals and firing from cell bodies in the locus coeruleus (Engberg and Eriksson, 1991). Guanfacine also promotes a downregulation of sympathomimetic outflow from the vasomotor center of the brain to the heart (Sica, 2007). Notably, extensive preclinical and clinical research has shown that both of these central and peripheral mechanisms may have a salient role in the reduction of cocaine craving, owing to the fact that activation of the lateral tegmental NE system Erb, 2010;Sinha et al, 2011;Mantsch et al, 2013) and autonomic peripheral arousal (Sinha et al, 2003;Fox et al, 2008b) are implicated in stress-induced motivation for, and relapse to, cocaine during early recovery.…”

Section: Introductionmentioning

confidence: 99%

Sex Differences in Guanfacine Effects on Drug Craving and Stress Arousal in Cocaine-Dependent Individuals

Fox

Morgan

Sinha

2014

Neuropsychopharmacol

103

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Currently, no FDA-approved medication exists for the treatment of cocaine use disorder. Furthermore, as women become increasingly more at risk for the consequences of cocaine addiction, the need to establish better-tailored treatment medications is paramount. We examine the effects of the alpha2 adrenergic agonist, guanfacine HCl, on responses to stress and drug cue in a group of cocainedependent men and women who also abuse alcohol and nicotine. Forty early abstinent treatment-seeking cocaine-dependent males and females were randomly assigned to receive either daily placebo (12 M/7 F) or guanfacine (2 or 3 mg) (15 M/6 F) for 3 weeks. In week 4, they participated in a laboratory experiment and were exposed to three 10-min guided imagery conditions (stress/stress, cue/cue, and stress/cue), one per day, consecutively in a random, counterbalanced order. Craving, negative emotion, anxiety, and cardiovascular function were assessed at baseline, immediately following imagery exposure, and at various recovery time points. Guanfacine significantly attenuated cocaine craving, alcohol craving, anxiety, and negative emotion following exposure to all three imagery conditions in females, but not males. Guanfacine did, however, reduce sympathetic tone as well as stress and cue-induced nicotine craving and systolic blood pressure (SBP) in both males and females. These findings highlight sex-specific effects of guanfacine on drug craving, anxiety, and negative mood with significant effects in women and not men. The findings suggest further evaluation of guanfacine in the treatment of cocaine use disorder with a specific focus on sex differences in treatment response.

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“…46 In humans, the plasma NE level may be elevated in some hypertensives, 47 and drugs that lower the plasma level of NE, such as clonidine and the other a2 adrenergic agonists, reduce blood pressure. 48 And a strain of spontaneously hypertensive rats shows elevations in both tissue NE levels and rates of chemically induced tumorigenesis. 49 A sixth line of evidence is that excessive body weight is associated with adrenoceptor polymorphisms and elevated blood NE, 50 and it is also a risk factor for some adult cancers.…”

Section: Literature Search Detailsmentioning

confidence: 99%

Is norepinephrine an etiological factor in some types of cancer?

Fitzgerald

2008

Intl Journal of Cancer

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I examine evidence that the signaling molecule norepinephrine (NE) is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) rodent studies of tumorigenesis in the context of NE manipulation; (ii) human studies of tricyclic antidepressant use and cancer rate; (iii) existence of pheochromocytoma, a cancer of the adrenal glands; (iv) cancer rate in families with individuals who have bipolar disorder; (v) hypertension and cancer risk; (vi) excessive body weight and cancer risk; and (vii) psychological stressors and cancer risk. Three aspects of the body's NE system are consistent with it playing an etiological role in various types of cancer: (i) NE circulates in the blood and can thereby access organ systems throughout the body, in addition to direct peripheral release by the sympathetic nervous system and being released within the brain; (ii) many of the body's organs possess NE receptors on the outer surface of at least some of their cells; (iii) by binding to its extracellular receptors, NE affects intracellular second messenger systems that could influence carcinogenesis. Most importantly, use of existing pharmaceutical drugs that either lower the level of NE (such as clonidine) or block NE receptors may lower the probability of an individual developing cancer, and this hypothesis could be tested immediately by an epidemiologist through examination of existing medical records. ' 2008 Wiley-Liss, Inc.Key words: norepinephrine; pharmacology; clonidine; adrenoceptor; rodent; hypertension; epidemiology; pheochromocytoma I present evidence that the signaling molecule norepinephrine (NE), which is a neurotransmitter and plays various roles in organs other than the brain, is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) in a series of rodent studies, increasing the level of NE in various organs increases tumorigenesis, whereas decreasing the level decreases tumorigenesis; (ii) in humans, tricyclic antidepressant use, which may boost the level of NE throughout the body, may be associated with increased rates of cancer; (iii) pheochromocytoma, which is a cancer of the adrenal glands, may be an example of NE causing cancer in the organ that releases it into the bloodstream; (iv) families with individuals who have bipolar disorder have elevated cancer rates, where bipolar disorder may be associated with a high level of NE; (v) hypertension is associated with an elevated level of NE in the bloodstream, and may be a cancer risk factor; (vi) excessive body weight is associated with elevated blood NE and is a cancer risk factor; and (vii) psychological stressors are associated with increased release of NE in the brain and bloodstream, and exposure to stress is potentially a cancer risk factor.In addition to the above evidence, including NE's role in the brain, several other aspects of the body's NE system are consistent with an etiological role in cancer: (i) In addition to relea...

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Centrally Acting Antihypertensive Agents: An Update

Cited by 93 publications

References 42 publications

Evaluating the carotid bodies and renal nerves as therapeutic targets for hypertension

Evaluating the carotid bodies and renal nerves as therapeutic targets for hypertension

Sex Differences in Guanfacine Effects on Drug Craving and Stress Arousal in Cocaine-Dependent Individuals

Is norepinephrine an etiological factor in some types of cancer?

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