The pathophysiology of hypertension
BMJ 2001; 322 doi: https://doi.org/10.1136/bmj.322.7291.912 (Published 14 April 2001) Cite this as: BMJ 2001;322:912All rapid responses
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In your article on the pathophysiology of hypertension,you mention
that "cross transplantational experiments with.....
..hypertensive rats......strongly suggests that hypertension has its
origins in the kidneys."
Were you referring to human hypertension or hypertension in rats?
The reasons for my question are as follows.
Rattus norvegicus has 42 chromosomes.
Chromosome numbers generally do not display any correlation with
evolutionary notions-i.e.surmised evolutionary hierarchical ranking.(see
www.kean.edu/~breid/chrom2.htm )
Mechanisms of meiotic cell division=sexual reproduction absolutely require
the synapsis of all chromosome pairs,and such synapsis requires an
absolute minimum degree of homology between members of each pair.A few
moments of careful thought lead to the inevitable conclusion that the
chromosome numbers of species are fixed-at least those of the sexually
reproductive members of species.
It is therefore quite implausible to entertain the notion that life as we
know it evolved.And therefore,any similarities in physiological or
pathological processes between species are entirely serendipitous,unless
they are the result of a common design-i.e.a creative act which was
designed in such a fashion as to comprise similar patterns of physiology
between species which we know to be genomically distinct.
In other words,the ingenuities of many gifted animal researchers have
produced a wealth of invaluable information,but the relevance of any such
information to humans remains an unknown quantity,until tested by
experiment.
There is a very sobering report in BMJ about FIALURIDIN which was found
safe for consumption by several different animal species,but certainly not
safe for human consumption.
It might be true to say that a significant quantum of scientific research
or design has been invalidated bythe invalid assumption that we share a
common evolutionary ancestry with other species.
Having said all that,I wish to thank you for maintaining such a marvellous
medical publication,and for granting as the opportunity to respond to your
articles.
Competing interests:
None declared
Competing interests: No competing interests
Re: The pathophysiology of hypertension : Micronutrients and Hypertension
Dear Editor,
The study by Beevers et al. is educational and interesting, and it thoroughly covers the patho-physiology of hypertension. [1] Here, we aim to underline the connection between diet intake of micronutrients and a number of non-communicable disorders, primarily hypertension [2].
The term "silent killer" refers to hypertension, which affects 1.28 billion people globally. Reduce the prevalence of hypertension by 33% between 2010 and 2030 is one of the worldwide non-communicable illness targets [3]. Micronutrient intervention in dietary patterns can lower blood pressure, stop or delay the development of hypertension, increase the effectiveness of antihypertensive medications, and minimise cardiovascular risk..The DASH (Dietary Approaches to Stop Hypertension) diet, has observed to lower the blood pressure significantly and is rich in vegetables, fruits and low fat dairy products and also recommends low sodium intake (below 100 mmol per day) [4]. Additionally, taking anti-hypertensive medications causes an individual's micronutrient levels to become unbalanced, making it imperative to follow a suitable diet rich in micronutrients. When taken orally, vitamins like vitamin A, vitamin C, iron, and magnesium have been found to have a negative correlation with diastolic blood pressure; this could be because nitric oxide is more readily available when given orally. Numerous research looking at the relationship between serum levels of vitamins A, C, and E and blood pressure has shown that antioxidant vitamin intake is important for the prevention of hypertension [5].
The majority of micronutrients are made up of minerals, and certain minerals, like selenium, are directly related to hypertension. Additionally, it has been discovered that drinking hard water, which contains calcium and magnesium carbonates, is associated with a lower risk of cardiovascular events [6]. No matter the patient's age or response to anti-hypertensive medication, an increased food intake can be linked to a higher prevalence of hypertension [7-8]. However, when vitamin C, vitamin E, and beta-carotene are added, there are no appreciable changes in blood pressure levels. Additionally, it has been noted that low intakes of copper and magnesium can enhance the prevalence of hypertension by 1.8–2 times, and that an optimal intake of zinc can control hypertension by altering renal Na+ transport[9–10]. Studies on hypertension primarily concentrate on electrolytes like sodium, magnesium, and potassium, but non-electrolytes like zinc, copper, and vitamins have also been found to have a direct or indirect impact on a person's blood pressure level. Selenium concentrate consumption in the diet also exhibits a clear relationship with blood pressure levels. Observations show that micronutrient levels in the food can modulate blood pressure levels, causing hypertension or regulating it.
References.
1. Beevers G, Lip GY, O'Brien E. ABC of hypertension: The pathophysiology of hypertension. BMJ. 2001 Apr 14;322(7291):912-6. doi: 10.1136/bmj.322.7291.912.
2. Chiplonkar SA, Agte VV, Tarwadi KV, Paknikar KM, Diwate UP. Micronutrient deficiencies as predisposing factors for hypertension in lacto-vegetarian Indian adults. J Am Coll Nutr. 2004 Jun;23(3):239-47. doi: 10.1080/07315724.2004.10719367. PMID: 15190049.
3. World Health Organization, Report on Hypertension available on https://www.who.int/health-topics/hypertension#tab=tab_1. [Accessed on 26 June 2022]
4. Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller 3rd ER, Simons-Morton DG, Karanja N, Lin PH; DASH-Sodium Collaborative Research Group: Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASHSodium Collaborative Research Group. N Engl J Med 344:3–10, 2001.
5. Shashi A. Chiplonkar PhD, Vaishali V. Agte PhD, Kirtan V. Tarwadi MSc, Kishor M. Paknikar PhD & Uma P. Diwate MD (2004) Micronutrient Deficiencies as Predisposing Factors for Hypertension in Lacto-Vegetarian Indian Adults, Journal of the American College of Nutrition, 23:3, 239-247, DOI: 10.1080/07315724.2004.10719367
6. Yousefi, M., Najafi Saleh, H., Yaseri, M., Jalilzadeh, M., &Mohammadi, A. A. (2019). Association of consumption of excess hard water, body mass index and waist circumference with risk of hypertension in individuals living in hard and soft water areas. Environmental geochemistry and health, 41(3), 1213–1221. https://doi.org/10.1007/s10653-018-0206-9
7. Chen J, He J, Hamm L, Batuman V, Whelton PK: Serum antioxidant vitamins and blood pressure in the United States population. Hypertension 40:810–816, 2002.
8. Laclaustra, M., Navas-Acien, A., Stranges, S., Ordovas, J. M., &Guallar, E. (2009). Serum selenium concentrations and hypertension in the US Population. Circulation. Cardiovascular quality and outcomes, 2(4), 369–376. https://doi.org/10.1161/CIRCOUTCOMES.108.831552
9. Williams, C. R., Mistry, M., Cheriyan, A. M., Williams, J. M., Naraine, M. K., Ellis, C. L., Mallick, R., Mistry, A. C., Gooch, J. L., Ko, B., Cai, H., & Hoover, R. S. (2019). Zinc deficiency induces hypertension by promoting renal Na+ reabsorption. American journal of physiology. Renal physiology, 316(4), F646–F653. https://doi.org/10.1152/ajprenal.00487.2018
10. Bastola, M.M., Locatis, C., Maisiak, R. et al. Selenium, copper, zinc and hypertension: an analysis of the National Health and Nutrition Examination Survey (2011–2016). BMC CardiovascDisord 20, 45 (2020). https://doi.org/10.1186/s12872-020-01355-x
Competing interests: No competing interests