Relationship between a genetic predisposition to hypertension, blood pressure levels and pain sensitivity

Pain ◽  
1999 ◽  
Vol 82 (3) ◽  
pp. 311-317 ◽  
Author(s):  
Luigina Guasti ◽  
Giovanni Gaudio ◽  
Danilo Zanotta ◽  
Paola Grimoldi ◽  
Maria Rosaria Petrozzino ◽  
...  
2009 ◽  
Vol 23 (3) ◽  
pp. 104-112 ◽  
Author(s):  
Stefan Duschek ◽  
Heike Heiss ◽  
Boriana Buechner ◽  
Rainer Schandry

Recent studies have revealed evidence for increased pain sensitivity in individuals with chronically low blood pressure. The present trial explored whether pain sensitivity can be reduced by pharmacological elevation of blood pressure. Effects of the sympathomimetic midodrine on threshold and tolerance to heat pain were examined in 52 hypotensive persons (mean blood pressure 96/61 mmHg) based on a randomized, placebo-controlled, double-blind design. Heat stimuli were applied to the forearm via a contact thermode. Confounding of drug effects on pain perception with changes in skin temperature, temperature sensitivity, and mood were statistically controlled for. Compared to placebo, higher pain threshold and tolerance, increased blood pressure, as well as reduced heart rate were observed under the sympathomimetic condition. Increases in systolic blood pressure between points of measurement correlated positively with increases in pain threshold and tolerance, and decreases in heart rate were associated with increases in pain threshold. The findings underline the causal role of hypotension in the augmented pain sensitivity related to this condition. Pain reduction as a function of heart rate decrease suggests involvement of a baroreceptor-related mechanism in the pain attrition. The increased proneness of persons with chronic hypotension toward clinical pain is discussed.


2010 ◽  
Author(s):  
Suzanne G. Helfer ◽  
Ashley D. Bugeja ◽  
Sarah E. Jackson ◽  
Elizabeth Woltja

2014 ◽  
Vol 2 (1) ◽  
pp. 13-17
Author(s):  
Pratik Akhani ◽  
Samir Mendpara ◽  
Bhupendra Palan

Background: Pain is one of the most common reasons for patients to seek medical attention and it causes considerable human suffering. Pain is a complex perception that differs enormously among individual patients. Gender plays an important role in how pain is experienced, coped with and treated. Even young healthy individuals often differ in how they perceive and cope with pain. This study was done to investigate gender differences in response to experimental pain among medical students from a western state in India. Methods: A total of 150 medical students (86 males and 64 females) participated in this interventional study. The Cold Pressor Test was used to exert experimental pain. To study the response, cardiovascular measures (radial pulse, systolic blood pressure and diastolic blood pressure) and pain sensitivity parameters (pain threshold, pain tolerance and pain rating) were assessed. Results: No significant difference was found in cardiovascular response to experimental pain between both the genders (p>0.05). Pain threshold and pain tolerance were found to be significantly higher in males whereas pain rating was found to be significantly higher in females (p<0.01). Pulse reactivity showed a negative relationship with pain threshold and pain tolerance whereas a positive relationship with pain rating, however no statistically significant relation was found between these measures. Conclusion: Females display greater pain sensitivity than males. Different pain perception might account for gender difference in pulse reactivity.


2018 ◽  
Vol 18 (3) ◽  
pp. 479-489 ◽  
Author(s):  
Kristian Kjær Petersen ◽  
Hjalte Holm Andersen ◽  
Masato Tsukamoto ◽  
Lincoln Tracy ◽  
Julian Koenig ◽  
...  

AbstractBackground and aimsThe autonomic nervous system (ANS) is capable of modulating pain. Aberrations in heart rate variability (HRV), reflective of ANS activity, are associated with experimental pain sensitivity, chronic pain, and more recently, pain modulatory mechanisms but the underlying mechanisms are still unclear. HRV is lowered during experimental pain as well as in chronic pain conditions and HRV can be increased by propranolol, which is a non-selective β-blocker. Sensitization of central pain pathways have been observed in several chronic pain conditions and human mechanistic pain biomarkers for these central pain pathways include temporal summation of pain (TSP) and conditioned pain modulation (CPM). The current study aimed to investigate the effect of the β-blocker propranolol, and subsequently assessing the response to standardized, quantitative, mechanistic pain biomarkers.MethodsIn this placebo-controlled, double-blinded, randomized crossover study, 25 healthy male volunteers (mean age 25.6 years) were randomized to receive 40 mg propranolol and 40 mg placebo. Heart rate, blood pressure, and HRV were assessed before and during experimental pain tests. Cuff pressure pain stimulation was used for assessment of pain detection (cPDTs) and pain tolerance (cPTTs) thresholds, TSP, and CPM. Offset analgesia (OA) was assessed using heat stimulation.ResultsPropranolol significantly reduced heart rate (p<0.001), blood pressure (p<0.02) and increased HRV (p<0.01) compared with placebo. No significant differences were found comparing cPDT (p>0.70), cPTT (p>0.93), TSP (p>0.70), OA-effect (p>0.87) or CPM (p>0.65) between propranolol and placebo.ConclusionsThe current study demonstrated that propranolol increased HRV, but did not affect pressure pain sensitivity or any pain facilitatory or modulatory outcomes.ImplicationsAnalgesic effects of propranolol have been reported in clinical pain populations and the results from the current study could indicate that increased HRV from propranolol is not associated with peripheral and central pain pathways in healthy male subjects.


Diabetes ◽  
2012 ◽  
Vol 61 (11) ◽  
pp. 3026-3032 ◽  
Author(s):  
Q. Qi ◽  
J. P. Forman ◽  
M. K. Jensen ◽  
A. Flint ◽  
G. C. Curhan ◽  
...  

Circulation ◽  
2018 ◽  
Vol 137 (7) ◽  
pp. 653-661 ◽  
Author(s):  
Raha Pazoki ◽  
Abbas Dehghan ◽  
Evangelos Evangelou ◽  
Helen Warren ◽  
He Gao ◽  
...  

2018 ◽  
Vol 36 ◽  
pp. e247-e248
Author(s):  
Adesola Oniyide ◽  
Olabode Akintoye ◽  
Bamidele Owoyele ◽  
Kehinde Olaniyi ◽  
Boluwatife Sola-Oniyide ◽  
...  

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