Laboratory Detection and Treatment of Primary Hypertension

Primary hypertension is defined as elevated blood pressure readings consistently exceeding 140/90 with no known causative conditions or factors. Presently, there are four categories of medications designed to treat hypertensive disorders from a conventional model. Based on their mode of action on cellular and systemic physiology, the categories are: 1. Thiazide diuretics; 2. Beta adrenergic blockers; 3. Angiotensin-converting enzyme inhibitors (ACE inhibitors) / Angiotensin II receptor blockers (ARBs); and 4. Calcium channel blockers (CCBs).

Recently, research has shown how several different nutrients share the properties and modes of action as these conventionally prescribed medications, making them therapeutic adjuncts, and in some cases, even replacements.

Diuretics

Commonly prescribed diuretics such as hydrochlorothiazide (HCT) and spironolactone are often the first line of defense in hypertensive cases.^1-3 By blocking sodium and chloride channels in the kidneys, urinary output is increased, resulting in lowered blood pressure.⁴

Nutrients exhibiting a diuretic effect on blood pressure regulation include: celery seed extract, dandelion root, parsley, cilantro, concentrated forms of vitamin C, the amino acid taurine, biotin, and the synthetic form of urea, referred to as carbamide.^5-7

Beta Adrenergic-Blocking Agents and Catecholamines

Common conventional medications such as metoprolol and propranolol have a mode of action designed to block the beta-adrenergic receptor sites along the vascular wall of the coronary vessels and heart muscle, inhibiting vascular constriction, thereby reducing heart rate and also reducing blood pressure.⁸

Nutrients showing beta adrenergic blocking effects include: choline, potassium, phosphatidylserine, GABA, L-theanine, and melatonin.^7,9,10-11

ACE Inhibitors and Receptor Blockers (ARBs)

Common generic medications such as lisinopril and benazepril act as inhibitors to the lung vasculature’s production of the angiotensin-converting enzyme. ACE production ensures a strong vasoconstricting response through the renin-angiotensin system (RAS). By inhibiting its production, or by blocking the ACE receptor site, vasodilation occurs, leading to reduced blood pressure and reduction of the ACE-dependent sodium and fluid retention hormones, aldosterone and anti-diuretic hormone (ADH), which normally elevate blood pressure.^12-13

Nutrients exhibiting an effect much like that of the ACE inhibitors and ARBs include: quercetin, fisetin, pycnogenol (pine bark extract), grape seed extract, and garlic.^7,14-15

Calcium Channel Blockers

Calcium channel blockers (CCBs), commonly identified by their names ending in “dipine,” such as amlodipine and nifedipine, reduce blood pressure by attaching to the calcium channel receptor of the blood vessel wall. By this action, the regular mechanism of calcium activating a vasoconstrictive response does not occur. This results in a vasodilation effect leading to lowered blood pressure.

Nutrients showing a calcium channel-blocking effect on the cardiovascular system include: magnesium, vitamin B₆, lipoic acid, steviosides, vitamin E, and the family of tocopherols.^7,16-17

By reducing the vasoconstriction effect, endothelial production of nitric oxide (eNO) can be produced, allowing for vascular dilation and lowered blood pressure. Nutrients having shown a direct effect on eNO production are: beets, hawthorn, glycine, resveratrol, and the L- forms of the amino acids arginine and citrulline.^7,18-19

Using Laboratory Testing to Determine Etiology

Routine lab testing such as a CBC with differential, CMP-14, TSH, fasting glucose, fasting insulin, and hemoglobin A1-C can often detect underlying conditions including metabolic syndrome, insulin resistance and renal disease, all of which commonly include a hypertensive component. However, when results are inconclusive, a more specific group of laboratory tests can be used to determine more precise discrepancies in blood pressure-regulating pathways, allowing for a more accurate diagnosis and treatment.

Angiotensin-Converting Enzyme – an enzyme produced by the pulmonary vascular endothelial cells which converts angiotensin I into the potent vasoconstrictor, angiotensin II, leading to hypertension.^13,20

Antidiuretic Hormone (ADH) – also known as vasopressin, this hypothalamic-produced hormone is released by the posterior pituitary gland and may increase vasoconstriction patterns by increasing the retention of sodium and water.^13,21

Aldosterone – a hormone produced by the adrenal cortex in response to fluctuations between potassium and sodium, which are greatly influenced by the production of angiotensin II in the renin-angiotensin-aldosterone system (RAAS).^12-13 Its release will temporarily increase blood pressure via retention of sodium and water.

Catecholamines (fractionated) – provides the levels of three forms of neurotransmitters having specific influence on blood pressure: norepinephrine and epinephrine (vasoconstrictors) and dopamine (vasodilator).²²

Dimethylarginine Asymmetric (ADMA) and Symmetric (SDMA) – two metabolites of L-arginine used to identify endothelial damage and inhibition of eNO. ADMA is associated with cardiovascular disease, while SDMA is associated with kidney disease.²³

C- Reactive Protein (high sensitivity) (CRP hs) – a liver-produced inflammatory protein that elevates in multiple conditions, including hypertension. By directly inhibiting endothelial nitric oxide synthase (eNOS) production, in addition to uncoupling its presence, vasoconstriction and hypertension are the result.²⁴

Magnesium RBC – a mineral needed for the relaxation of smooth and skeletal muscle. A natural calcium channel blocker, it increases nitric oxide and vasodilation.²⁵

Other Useful Tests

B-Type Natriuretic Peptide (BNP) – a peptide produced by cardiac myocytes in response to stress on the cardiac muscle wall. It produces a diuretic effect, reducing blood pressure in an attempt to normalize cardiac function.²⁶

Renin – a glycoprotein secreted by the kidney which can also increase production of angiotensin II, resulting in vasoconstriction.^12-13,20

Cortisol – this adrenal cortex hormone decreases vasodilation by inhibiting cholinergic pathways, resulting in vasoconstriction.^27-28

Hypertension is at epidemic proportions and can be caused by a multitude of conditions of known and unknown origins. With the use of basic blood chemistry testing, in addition to more specific blood chemistry markers, the clinician is able to evaluate several different systems and biochemical pathways that contribute to and influence blood pressure regulation, giving him/her more diagnostic confidence when prescribing a treatment with conventional methods or an alternative approach.

References

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